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Transactivation of the mouse sulfonylurea receptor I gene by BETA2/NeuroD.

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dc.contributor.authorKim, JW-
dc.contributor.authorSeghers, V-
dc.contributor.authorCho, JH-
dc.contributor.authorKang, Y-
dc.contributor.authorKim, S-
dc.contributor.authorRyu, Y-
dc.contributor.authorBaek, K-
dc.contributor.authorAguilar-Bryan, L-
dc.contributor.authorLee, YD-
dc.contributor.authorBryan, J-
dc.contributor.authorSuh-Kim, H-
dc.date.accessioned2011-07-18T05:38:17Z-
dc.date.available2011-07-18T05:38:17Z-
dc.date.issued2002-
dc.identifier.issn0888-8809-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3408-
dc.description.abstractThe sulfonylurea receptor 1 (SUR1) plays a key role in regulation of insulin secretion in pancreatic beta-cells. In this study we investigated the mechanism for tissue-specific expression of the SUR1 gene. A -138/-20 fragment exhibited basal promoter activity while the -660/-20 fragment contained a regulatory element for tissue-specific expression of the mouse SUR1 gene. A pancreatic beta-cell-specific transcription factor, BETA2 (beta-cell E box transcription factor)/NeuroD, enhanced the promoter activity of the -660/-20 fragment in cooperation with E47. Coexpression of a dominant negative mutant of BETA2/NeuroD, BETA2(1-233), repressed the promoter activity of the -660/-20 fragment. BETA2/NeuroD bound specifically to the E3 element located at -141. The E3 sequence in a heterologous context conferred transactivation by BETA2/NeuroD in HeLa and HIT cells. Mutation of E3 eliminated the stimulatory effect of BETA2/NeuroD. Unlike BETA2/NeuroD, neurogenin 3 (ngn3) could not activate the E3 element in HeLa cells. Overexpression of ngn3 concomitantly increased expression of BETA2/NeuroD and SUR1 in HIT cells but not in HeLa cells. These results indicate that BETA2/NeuroD induces tissue-specific expression of the SUR1 gene through the E3 element. These results also suggest that E3 is specific for BETA2/NeuroD, and the stimulatory effect of ngn3 in HIT cells may require factors specifically expressed in HIT cells.-
dc.language.isoen-
dc.subject.MESHATP-Binding Cassette Transporters-
dc.subject.MESHAnimals-
dc.subject.MESHBase Sequence-
dc.subject.MESHBasic Helix-Loop-Helix Transcription Factors-
dc.subject.MESHBinding Sites-
dc.subject.MESHDNA-Binding Proteins-
dc.subject.MESHGene Expression-
dc.subject.MESHHela Cells-
dc.subject.MESHHumans-
dc.subject.MESHInsulinoma-
dc.subject.MESHMice-
dc.subject.MESHMolecular Sequence Data-
dc.subject.MESHMutagenesis-
dc.subject.MESHPancreatic Neoplasms-
dc.subject.MESHPeptide Fragments-
dc.subject.MESHPotassium Channels-
dc.subject.MESHPotassium Channels, Inwardly Rectifying-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHRats-
dc.subject.MESHReceptors, Drug-
dc.subject.MESHRegulatory Sequences, Nucleic Acid-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHTrans-Activators-
dc.subject.MESHTranscriptional Activation-
dc.subject.MESHTransfection-
dc.subject.MESHTumor Cells, Cultured-
dc.titleTransactivation of the mouse sulfonylurea receptor I gene by BETA2/NeuroD.-
dc.typeArticle-
dc.identifier.pmid11981044-
dc.identifier.urlhttp://mend.endojournals.org/cgi/pmidlookup?view=long&pmid=11981044-
dc.contributor.affiliatedAuthor강, 엽-
dc.contributor.affiliatedAuthor이, 영돈-
dc.contributor.affiliatedAuthor서, 해영-
dc.type.localJournal Papers-
dc.identifier.doi10.1210/mend.16.5.0934-
dc.citation.titleMolecular endocrinology (Baltimore, Md.)-
dc.citation.volume16-
dc.citation.number5-
dc.citation.date2002-
dc.citation.startPage1097-
dc.citation.endPage1107-
dc.identifier.bibliographicCitationMolecular endocrinology (Baltimore, Md.), 16(5). : 1097-1107, 2002-
dc.identifier.eissn1944-9917-
dc.relation.journalidJ008888809-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Journal Papers > School of Medicine / Graduate School of Medicine > Anatomy
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