Promoters for the human alcohol dehydrogenases genes ADH1, ADH2 , and ADH3 : interaction of CCAAT/enhancer-binding protein with elements flanking the ADH2 TATA box
Identifieur interne : 001F46 ( Istex/Checkpoint ); précédent : 001F45; suivant : 001F47Promoters for the human alcohol dehydrogenases genes ADH1, ADH2 , and ADH3 : interaction of CCAAT/enhancer-binding protein with elements flanking the ADH2 TATA box
Auteurs : Mark J. Stewart [États-Unis] ; M. Scott Mcbride [États-Unis] ; Laurie A. Winter [États-Unis] ; Gregg Duester [États-Unis]Source :
- Gene [ 0378-1119 ] ; 1990.
English descriptors
- Teeft :
- Adh2, Adh2 promoter, Adh3, Adh3 genes, Adhi, Assay, Binding sites, Codon, Dehydrogenase, Dnase, Duester, Early promoter, Encoding, Enhancer, Fiver, Footprint, Footprint analysis, Footprinting, Gene, Gene expression, Gene family, Hep3b, Hepatoma, Hepatoma cell lines, Hepg2, Human adh2 gene, Human fiver, Human liver, Human liver alcohol dehydrogenase, Landschulz, Mcknight, Mrna, Nuclear extracts, Nucleotide sequences, Plasmid, Primer, Primer extension, Primer extension analyses, Promoter, Sequence identity, Tata, Tfiid, Transcription, Transcription factors, Transcriptional, Transcriptional machinery, Transfection.
Abstract
Abstract: The human ADH1, ADH2, and ADH3 genes are closely related members of a gene family which are differentially expressed during liver development. To begin examining the mechanism of this tissue-specific and stage-specific expression, the 5′-flanking nucleotide (nt) sequences of the three genes were determined and the transcription start points (tsp) were identified. Sequences of all three genes indicated a high degree of homology (>80% nt sequence identity) from the AUG translation start codon to about nt −780 relative to the tsp. Transiwnt transfection assays of a set of plasmids containing various lengths of ADH 5′-flanking DNA fused to cat were performed in the HepG2 and Hep3B human hepatoma cell lines. The results indicated that the ADH2 promoter-proximal region was transcriptionally active in the absence of upstream sequences. To identify potential cis-acting elements in the ADH2 promoter-proximal region, a DNase I footprinting assay using a rat liver nuclear extract was used. Protection occurred in several locations including one, between nt −51 and −10, which shares homology with known binding sites for a previously identified rat-liver transcription factor called CCAAT/enhancer binding protein (C/EBP). Purified C/EBP was shown by footprint analysis to bind at two distinct sites in the ADH2 promoter located at nt −51 to −31 and −21 to −10. The TATA-box promoter element at nt −30 to −22 was not protected by C/EBP, but was partially protected by a factor in the rat liver nuclear extract. Thus, it is possible that the flanking C/EBP molecules may create a novel binding pocket for TFIID, the TATA-binding general transcription factor for RNA polymerase II. Alternatively, the C/EBP molecules may block access to the TATA box, and stimulate transcription of ADH2 by interacting with some component(s) other than TFIID.
Url:
DOI: 10.1016/0378-1119(90)90190-3
Affiliations:
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Winter</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Colorado State University, Fort Collins, CO 80523</wicri:regionArea><wicri:noRegion>CO 80523</wicri:noRegion></affiliation></author><author><name sortKey="Duester, Gregg" sort="Duester, Gregg" uniqKey="Duester G" first="Gregg" last="Duester">Gregg Duester</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry, Colorado State University, Fort Collins, CO 80523</wicri:regionArea><wicri:noRegion>CO 80523</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Gene</title><title level="j" type="abbrev">GENE</title><idno type="ISSN">0378-1119</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1990">1990</date><biblScope unit="volume">90</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="271">271</biblScope><biblScope unit="page" to="279">279</biblScope></imprint><idno type="ISSN">0378-1119</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0378-1119</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adh2</term><term>Adh2 promoter</term><term>Adh3</term><term>Adh3 genes</term><term>Adhi</term><term>Assay</term><term>Binding sites</term><term>Codon</term><term>Dehydrogenase</term><term>Dnase</term><term>Duester</term><term>Early promoter</term><term>Encoding</term><term>Enhancer</term><term>Fiver</term><term>Footprint</term><term>Footprint analysis</term><term>Footprinting</term><term>Gene</term><term>Gene expression</term><term>Gene family</term><term>Hep3b</term><term>Hepatoma</term><term>Hepatoma cell lines</term><term>Hepg2</term><term>Human adh2 gene</term><term>Human fiver</term><term>Human liver</term><term>Human liver alcohol dehydrogenase</term><term>Landschulz</term><term>Mcknight</term><term>Mrna</term><term>Nuclear extracts</term><term>Nucleotide sequences</term><term>Plasmid</term><term>Primer</term><term>Primer extension</term><term>Primer extension analyses</term><term>Promoter</term><term>Sequence identity</term><term>Tata</term><term>Tfiid</term><term>Transcription</term><term>Transcription factors</term><term>Transcriptional</term><term>Transcriptional machinery</term><term>Transfection</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The human ADH1, ADH2, and ADH3 genes are closely related members of a gene family which are differentially expressed during liver development. To begin examining the mechanism of this tissue-specific and stage-specific expression, the 5′-flanking nucleotide (nt) sequences of the three genes were determined and the transcription start points (tsp) were identified. Sequences of all three genes indicated a high degree of homology (>80% nt sequence identity) from the AUG translation start codon to about nt −780 relative to the tsp. Transiwnt transfection assays of a set of plasmids containing various lengths of ADH 5′-flanking DNA fused to cat were performed in the HepG2 and Hep3B human hepatoma cell lines. The results indicated that the ADH2 promoter-proximal region was transcriptionally active in the absence of upstream sequences. To identify potential cis-acting elements in the ADH2 promoter-proximal region, a DNase I footprinting assay using a rat liver nuclear extract was used. Protection occurred in several locations including one, between nt −51 and −10, which shares homology with known binding sites for a previously identified rat-liver transcription factor called CCAAT/enhancer binding protein (C/EBP). Purified C/EBP was shown by footprint analysis to bind at two distinct sites in the ADH2 promoter located at nt −51 to −31 and −21 to −10. The TATA-box promoter element at nt −30 to −22 was not protected by C/EBP, but was partially protected by a factor in the rat liver nuclear extract. Thus, it is possible that the flanking C/EBP molecules may create a novel binding pocket for TFIID, the TATA-binding general transcription factor for RNA polymerase II. Alternatively, the C/EBP molecules may block access to the TATA box, and stimulate transcription of ADH2 by interacting with some component(s) other than TFIID.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Stewart, Mark J" sort="Stewart, Mark J" uniqKey="Stewart M" first="Mark J." last="Stewart">Mark J. Stewart</name></noRegion><name sortKey="Duester, Gregg" sort="Duester, Gregg" uniqKey="Duester G" first="Gregg" last="Duester">Gregg Duester</name><name sortKey="Scott Mcbride, M" sort="Scott Mcbride, M" uniqKey="Scott Mcbride M" first="M." last="Scott Mcbride">M. Scott Mcbride</name><name sortKey="Winter, Laurie A" sort="Winter, Laurie A" uniqKey="Winter L" first="Laurie A." last="Winter">Laurie A. Winter</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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