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Idenitification and functional characterization of the peroxisomal proliferator response element in rat GLUT2 promoter

DC Field Value Language
dc.contributor.author안용호-
dc.date.accessioned2019-11-11T05:06:41Z-
dc.date.available2019-11-11T05:06:41Z-
dc.date.issued2000-
dc.identifier.issn0012-1797-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/171620-
dc.description.abstractWe identified the peroxisomal proliferator response element (PPRE) in the +68/+89 region of the rat GLUT2 gene. To identify whether the putative PPRE in the GLUT2 gene (GLUT2-PPRE) is functional, GLUT2 promoter-luciferase reporter constructs were transfected into CV-1 cells. Promoter activities were increased by coexpression of peroxisomal proliferator-activated receptor (PPAR)-gamma, retinoid X receptor (RXR)-alpha, and treatment of their ligands; troglitazone and 9-cis retinoic acid potentiated the transactivational effects. Introduction of mutations in GLUT2-PPRE resulted in loss of transactivational effects of the PPAR-gamma/RXR-alpha heterodimer. Electrophoretic mobility shift assay using nuclear extracts of CV-1 cells, which were transfected with various combinations of PPARs or RXR-alpha expression plasmids, revealed that heterodimers of PPAR-gamma and RXR-alpha preferentially bound to GLUT2-PPRE. In HIT-T15 cells, promoter activity of the rat GLUT2 gene was increased by troglitazone and 9-cis retinoic acid, and mutations of GLUT2-PPRE resulted in reduction of promoter activity. In addition, we observed increased GLUT2 transcription by troglitazone and 9-cis retinoic acid in isolated rat primary islets. These results suggested that the GLUT2-PPRE is functional and plays a significant role in gene expression of GLUT2 in pancreatic beta-cells. This is the first report identifying PPRE in a gene involved in glucose homeostasis, linking the effect of troglitazone on the regulation of insulin secretion.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherAmerican Diabetes Association-
dc.relation.isPartOfDiabetes-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAnimals-
dc.subject.MESHBase Sequence-
dc.subject.MESHCell Line-
dc.subject.MESHCells, Cultured-
dc.subject.MESHChromans/pharmacology-
dc.subject.MESHConsensus Sequence-
dc.subject.MESHDNA-Binding Proteins/chemistry-
dc.subject.MESHDNA-Binding Proteins/metabolism-
dc.subject.MESHDimerization-
dc.subject.MESHGene Expression Regulation*/drug effects-
dc.subject.MESHGlucose Transporter Type 2-
dc.subject.MESHHypoglycemic Agents/pharmacology-
dc.subject.MESHIslets of Langerhans/drug effects-
dc.subject.MESHIslets of Langerhans/metabolism*-
dc.subject.MESHMale-
dc.subject.MESHMonosaccharide Transport Proteins/genetics*-
dc.subject.MESHPromoter Regions, Genetic*-
dc.subject.MESHProtein Multimerization-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/chemistry-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/genetics-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/metabolism*-
dc.subject.MESHReceptors, Retinoic Acid/metabolism-
dc.subject.MESHRecombinant Fusion Proteins/biosynthesis-
dc.subject.MESHRecombinant Proteins/metabolism-
dc.subject.MESHRetinoid X Receptors-
dc.subject.MESHSequence Alignment-
dc.subject.MESHThiazoles/pharmacology-
dc.subject.MESHThiazolidinediones*-
dc.subject.MESHTranscription Factors/chemistry-
dc.subject.MESHTranscription Factors/genetics-
dc.subject.MESHTranscription Factors/metabolism*-
dc.subject.MESHTranscription, Genetic/drug effects-
dc.subject.MESHTransfection-
dc.subject.MESHTretinoin/pharmacology-
dc.titleIdenitification and functional characterization of the peroxisomal proliferator response element in rat GLUT2 promoter-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry and Molecular Biology (생화학-분자생물학교실)-
dc.contributor.googleauthorH I Kim-
dc.contributor.googleauthorJ W Kim-
dc.contributor.googleauthorS H Kim-
dc.contributor.googleauthorJ Y Cha-
dc.contributor.googleauthorK S Kim-
dc.contributor.googleauthorY H Ahn-
dc.identifier.doi10.2337/diabetes.49.9.1517-
dc.contributor.localIdA02249-
dc.relation.journalcodeJ00718-
dc.identifier.eissn1939-327X-
dc.identifier.pmid10969836-
dc.identifier.urlhttp://diabetes.diabetesjournals.org/content/49/9/1517-
dc.subject.keywordWe identified the peroxisomal proliferator response element (PPRE) in the +68/+89 region of the rat GLUT2 gene. To identify whether the putative PPRE in the GLUT2 gene (GLUT2-PPRE) is functional, GLUT2 promoter-luciferase reporter constructs were transfected into CV-1 cells. Promoter activities were increased by coexpression of peroxisomal proliferator-activated receptor (PPAR)-gamma, retinoid X receptor (RXR)-alpha, and treatment of their ligands-
dc.subject.keywordtroglitazone and 9-cis retinoic acid potentiated the transactivational effects. Introduction of mutations in GLUT2-PPRE resulted in loss of transactivational effects of the PPAR-gamma/RXR-alpha heterodimer. Electrophoretic mobility shift assay using nuclear extracts of CV-1 cells, which were transfected with various combinations of PPARs or RXR-alpha expression plasmids, revealed that heterodimers of PPAR-gamma and RXR-alpha preferentially bound to GLUT2-PPRE. In HIT-T15 cells, promoter activity of the rat GLUT2 gene was increased by troglitazone and 9-cis retinoic acid, and mutations of GLUT2-PPRE resulted in reduction of promoter activity. In addition, we observed increased GLUT2 transcription by troglitazone and 9-cis retinoic acid in isolated rat primary islets. These results suggested that the GLUT2-PPRE is functional and plays a significant role in gene expression of GLUT2 in pancreatic beta-cells. This is the first report identifying PPRE in a gene involved in glucose homeostasis, linking the effect of troglitazone on the regulation of insulin secretion.-
dc.contributor.alternativeNameAhn, Yong Ho-
dc.contributor.affiliatedAuthor안용호-
dc.citation.volume49-
dc.citation.number9-
dc.citation.startPage1517-
dc.citation.endPage1524-
dc.identifier.bibliographicCitationDiabetes, Vol.49(9) : 1517-1524, 2000-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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