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Tumor necrosis factor-alpha and interleukin-1 beta increases CTRP1 expression in adipose tissue

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dc.contributor.authorKim, Kun-yong-
dc.contributor.authorKim, Hwa Young-
dc.contributor.authorKim, Jae Hyeong-
dc.contributor.authorLee, Chul-Ho-
dc.contributor.authorKim, Do-Hyung-
dc.contributor.authorLee, Young Ho-
dc.contributor.authorHan, Seung Hyun-
dc.contributor.authorLim, Jong-Seok-
dc.contributor.authorCho, Dae Ho-
dc.contributor.authorLee, Myeong-Sok-
dc.contributor.authorYoon, Sukjoon-
dc.contributor.authorKim, Keun Il-
dc.contributor.authorYoon, Do-Young-
dc.contributor.authorYang, Young-
dc.date.available2021-02-22T11:17:05Z-
dc.date.issued2006-07-
dc.identifier.issn0014-5793-
dc.identifier.issn1873-3468-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8806-
dc.description.abstractCTRP1, a member of the CTRP superfamily, consists of an N-terminal signal peptide sequence followed by a variable region, a collagen repeat domain, and a C-terminal globular domain. CTRP1 is expressed at high levels in adipose tissues of LPS-stimulated Sprague-Dawley rats. The LPS-induced increase in CTRP1 gene expression was found to be mediated by TNF-alpha and IL-1 beta. Also, a high level of expression of CTRP1 mRNA was observed in adipose tissues of Zucker diabetic fatty (falfa) rats, compared to Sprague-Dawley rats in the absence of LPS stimulation. These findings indicate that CTRP1 expression may be associated with a low-grade chronic inflammation status in adipose tissues. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherELSEVIER SCIENCE BV-
dc.titleTumor necrosis factor-alpha and interleukin-1 beta increases CTRP1 expression in adipose tissue-
dc.typeArticle-
dc.publisher.location네델란드-
dc.identifier.doi10.1016/j.febslet.2006.06.034-
dc.identifier.scopusid2-s2.0-33745386896-
dc.identifier.wosid000238964800031-
dc.identifier.bibliographicCitationFEBS LETTERS, v.580, no.16, pp 3953 - 3960-
dc.citation.titleFEBS LETTERS-
dc.citation.volume580-
dc.citation.number16-
dc.citation.startPage3953-
dc.citation.endPage3960-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusRESISTIN GENE-EXPRESSION-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlus3T3-L1 ADIPOCYTES-
dc.subject.keywordPlusMOLECULAR-CLONING-
dc.subject.keywordPlusWEIGHT-LOSS-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusOBESITY-
dc.subject.keywordPlusFAT-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusPRODUCT-
dc.subject.keywordAuthoradipokine-
dc.subject.keywordAuthorproinflammatory cytokines-
dc.subject.keywordAuthorCTRP-
dc.identifier.urlhttps://febs.onlinelibrary.wiley.com/doi/full/10.1016/j.febslet.2006.06.034-
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이과대학 > 생명시스템학부 > 1. Journal Articles

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