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Cited 29 time in webofscience Cited 31 time in scopus
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Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-kappa B activation

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dc.contributor.authorKim, Dae-Seok-
dc.contributor.authorKim, Bora-
dc.contributor.authorTahk, Hongmin-
dc.contributor.authorKim, Dong-Hyun-
dc.contributor.authorAhn, Eu-Ree-
dc.contributor.authorChoi, Changsun-
dc.contributor.authorJeon, Yoon-
dc.contributor.authorPark, Seo Young-
dc.contributor.authorLee, Ho-
dc.contributor.authorOh, Seung Hyun-
dc.contributor.authorKim, Soo-Youl-
dc.date.available2019-05-30T00:36:21Z-
dc.date.issued2010-12-
dc.identifier.issn0006-291X-
dc.identifier.issn1090-2104-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22008-
dc.description.abstractTransglutaminase 2 knockout (TGase2(-/-)) mice show significantly reduced inflammation with decreased myofibroblasts in a unilateral ureteral obstruction (UUO) model, but the mechanism remains to be clarified. Nuclear factor-kappa B (NF-kappa B) activation plays a major role in the progression of inflammation in an obstructive nephropathy model. However, the key factors extending the duration of NF-kappa B activation in UUO are not known. In several inflammatory diseases, we and others recently found that TGase 2 plays a key role in extending NF-kappa B activation, which contributes to the pathogenesis of disease. In the current study, we found that NF-kappa B activity in mouse embryogenic fibroblasts (MEFs) from TGase2(-/-) mice remained at the control level while the NF-kappa B activity of wild-type (WT) MEFs was highly increased under hypoxic stress. Using the obstructive nephropathy model, we found that NF-kappa B activity remained at the control level in TGase2(-/-) mouse kidney tissues, as measured by COX-2 expression, but was highly increased in WT tissues. We conclude that TGase 2 gene ablation reduces the duration of NF-kappa B activation in ischemic injury. (C) 2010 Elsevier Inc. All rights reserved.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.titleTransglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-kappa B activation-
dc.typeArticle-
dc.identifier.doi10.1016/j.bbrc.2010.11.063-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.403, no.3-4, pp 479 - 484-
dc.description.isOpenAccessN-
dc.identifier.wosid000286021300040-
dc.identifier.scopusid2-s2.0-78650170689-
dc.citation.endPage484-
dc.citation.number3-4-
dc.citation.startPage479-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume403-
dc.type.docTypeArticle-
dc.publisher.location미국-
dc.subject.keywordAuthorTransglutaminase 2-
dc.subject.keywordAuthorTransglutaminase 2 knockout mouse-
dc.subject.keywordAuthorUnilateral ureteral obstruction-
dc.subject.keywordAuthorIschemia-
dc.subject.keywordAuthorNuclear factor-kappa B-
dc.subject.keywordAuthorRenal injury-
dc.subject.keywordPlusUNILATERAL URETERAL OBSTRUCTION-
dc.subject.keywordPlusCHRONIC KIDNEY-DISEASE-
dc.subject.keywordPlusTISSUE TRANSGLUTAMINASE-
dc.subject.keywordPlusDIABETIC-NEPHROPATHY-
dc.subject.keywordPlusEXTRACELLULAR-MATRIX-
dc.subject.keywordPlusBLOOD MONOCYTES-
dc.subject.keywordPlusTGF-BETA-
dc.subject.keywordPlusFIBROSIS-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusMODEL-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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