Brazilin inhibits activities of protein kinase C and insulin receptor serine kinase in rat liver

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dc.contributor.authorKim, SGko
dc.contributor.authorKim, You-Meko
dc.contributor.authorKhil, LYko
dc.contributor.authorJeon, SDko
dc.contributor.authorSo, DSko
dc.contributor.authorMoon, CHko
dc.contributor.authorMoon, CKko
dc.date.accessioned2018-03-23T00:19:02Z-
dc.date.available2018-03-23T00:19:02Z-
dc.date.created2018-03-15-
dc.date.created2018-03-15-
dc.date.issued1998-04-
dc.identifier.citationARCHIVES OF PHARMACAL RESEARCH, v.21, no.2, pp.140 - 146-
dc.identifier.issn0253-6269-
dc.identifier.urihttp://hdl.handle.net/10203/241000-
dc.description.abstractHypoglycemic action of brazilin was found to be based on the improvement of peripheral glucose utility, and this action might be correlated with the insulin action pathway. In the present study we investigated the effect of brazilin on the insulin receptor autophosphorylation protein kinase C (PKC), protein phosphatase and insulin receptor serine kinase in order to confirm whether the hypoglycemic mechanism is concerned with insulin action pathway. Brazilin was found to inhibit PKC and insulin receptor serine kinase, which are involved in the regulation of insulin signal pathway. But any significant effect was not shown on insulin receptor tyrosine kinase activity, autophosphorylation and phosphatase activity. These findings suggest that brazilin might enhance insulin receptor function by decreasing serine phosphorylation, which might mediate hypoglycemic effect of brazilin.-
dc.languageEnglish-
dc.publisherPHARMACEUTICAL SOC KOREA-
dc.subjectTYROSINE KINASE-
dc.subjectPHORBOL ESTERS-
dc.subjectGLUCOSE-TRANSPORT-
dc.subjectPHOSPHORYLATION-
dc.subjectADIPOCYTES-
dc.subjectAUTOPHOSPHORYLATION-
dc.subjectPHOSPHATASES-
dc.subjectSTIMULATE-
dc.subjectBINDING-
dc.subjectCELLS-
dc.titleBrazilin inhibits activities of protein kinase C and insulin receptor serine kinase in rat liver-
dc.typeArticle-
dc.identifier.wosid000073103200007-
dc.identifier.scopusid2-s2.0-0032035193-
dc.type.rimsART-
dc.citation.volume21-
dc.citation.issue2-
dc.citation.beginningpage140-
dc.citation.endingpage146-
dc.citation.publicationnameARCHIVES OF PHARMACAL RESEARCH-
dc.identifier.doi10.1007/BF02974018-
dc.contributor.localauthorKim, You-Me-
dc.contributor.nonIdAuthorKim, SG-
dc.contributor.nonIdAuthorKhil, LY-
dc.contributor.nonIdAuthorJeon, SD-
dc.contributor.nonIdAuthorSo, DS-
dc.contributor.nonIdAuthorMoon, CH-
dc.contributor.nonIdAuthorMoon, CK-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorBrazilin-
dc.subject.keywordAuthorinsulin receptor-
dc.subject.keywordAuthorautophosphorylation-
dc.subject.keywordAuthorprotein kinase C-
dc.subject.keywordAuthorserine kinase-
dc.subject.keywordAuthorliver-
dc.subject.keywordPlusTYROSINE KINASE-
dc.subject.keywordPlusPHORBOL ESTERS-
dc.subject.keywordPlusGLUCOSE-TRANSPORT-
dc.subject.keywordPlusPHOSPHORYLATION-
dc.subject.keywordPlusADIPOCYTES-
dc.subject.keywordPlusAUTOPHOSPHORYLATION-
dc.subject.keywordPlusPHOSPHATASES-
dc.subject.keywordPlusSTIMULATE-
dc.subject.keywordPlusBINDING-
dc.subject.keywordPlusCELLS-
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