Elements in the distal 5'-flanking sequence and the first intron function cooperatively to regulate glutamine synthetase transcription during adipocyte differentiation
DC Field | Value | Language |
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dc.contributor.author | Hadden, Timothy J. | - |
dc.contributor.author | Ryou, Chongsuk | - |
dc.contributor.author | Miller, Richard E. | - |
dc.date.accessioned | 2021-06-24T01:09:02Z | - |
dc.date.available | 2021-06-24T01:09:02Z | - |
dc.date.created | 2021-01-21 | - |
dc.date.issued | 1997-10 | - |
dc.identifier.issn | 0305-1048 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/47028 | - |
dc.description.abstract | Glutamine synthetase (QS) expression increases dramatically during adipocyte differentiation of confluent 3T3-L1 cells. To identify differentiation-responsive cis-acting elements in the GS gene, several GS fusion genes were prepared and analyzed in stably transfected 3T3-L1 cells under conditions that trigger adipocyte differentiation. We find that the GS proximal 5'-flanking sequence lacks the regulatory elements required for differentiation-responsive expression. In contrast, a 2 kb intron 1 restriction fragment fused upstream of a heterologous promoter does drive reporter gene expression during hormone-triggered differentiation. The enhancer activity was localized to a 310 bp sequence near the middle of intron 1. Expression of fusion genes that include this 310 bp sequence does not temporally coincide with native gene expression. However, a composite gene that includes a far upstream GS sequence and the 2 kb intron 1 sequence yields a qualitatively different pattern of expression that closely resembles that of the native GS gene. The far upstream sequence alone exhibits no enhancer activity, Electrophoretic mobility shift analyses indicate that a 32 bp sequence within the 310 bp functional enhancer specifically binds differentiation-associated nuclear proteins. Although a C/EBP consensus sequence occurs in the 32 bp fragment, supershift analyses exclude C/EBP isoforms as the binding factor. In contrast, mutational analysis of the putative enhancer suggests that an HNF-3 isoform is involved. Thus our data indicate that elements in the distal 5'-flanking sequence and the first intron function cooperatively to regulate GS transcription and that HNF-3 may participate in that regulation. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | Oxford University Press | - |
dc.title | Elements in the distal 5'-flanking sequence and the first intron function cooperatively to regulate glutamine synthetase transcription during adipocyte differentiation | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ryou, Chongsuk | - |
dc.identifier.doi | 10.1093/nar/25.19.3930 | - |
dc.identifier.scopusid | 2-s2.0-0030963739 | - |
dc.identifier.wosid | A1997XZ39800026 | - |
dc.identifier.bibliographicCitation | Nucleic Acids Research, v.25, no.19, pp.3930 - 3936 | - |
dc.relation.isPartOf | Nucleic Acids Research | - |
dc.citation.title | Nucleic Acids Research | - |
dc.citation.volume | 25 | - |
dc.citation.number | 19 | - |
dc.citation.startPage | 3930 | - |
dc.citation.endPage | 3936 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | CULTURED 3T3-L1 ADIPOCYTES | - |
dc.subject.keywordPlus | DIBUTYRYL-CYCLIC-AMP | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | INSULIN | - |
dc.subject.keywordPlus | HYDROCORTISONE | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | DECREASES | - |
dc.subject.keywordPlus | BINDING | - |
dc.identifier.url | https://academic.oup.com/nar/article/25/19/3930/2549209 | - |
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