Inhibition in vitro transcription by specific double-stranded oligodeoxyribonucleotides
Identifieur interne : 001F56 ( Istex/Checkpoint ); précédent : 001F55; suivant : 001F57Inhibition in vitro transcription by specific double-stranded oligodeoxyribonucleotides
Auteurs : Henry Wu [États-Unis] ; John S. Holcenberg [États-Unis] ; John Tomich [États-Unis] ; Jeannie Chen [États-Unis] ; Peter A. Jones [États-Unis] ; Sheng-He Huang [États-Unis] ; Kathryn L. Calame [États-Unis]Source :
- Gene [ 0378-1119 ] ; 1990.
English descriptors
- Teeft :
- Activates transcription, Antisense oligos, Aqueous phase, Assay, Binding factors, Binding proteins, Binding site, Biosystems user bulletin, Cancer center, Childrens hospital, Complementary overhangs, Control expression, Control transcription, Cooperative interactions, Enhancer elements, Functional assay, Hela cells, Higher concentrations, Inhibition, Inhibitor, Methylation, Molar, Molar ratio, Molt4 cells, Nuclear binding factors, Nuclear extracts, Nucleic acids, Oligo, Oligo length, Oligos, Phosphodiester linkage, Primer, Primer extension, Promoter, Schmidt, Specific genes, Splx2b, Tata, Therapeutic approach, Tjian, Transcription, Transcriptional, Transcriptional factor, Transcriptional unit, Tris buffer, Unique factors, Upper strand, Whole cells.
Abstract
Abstract: A potential new therapeutic approach to control gene expression is the use of double-stranded (ds) oligodeoxyribonucleotides (oligos) to compete for the binding of nuclear factors to specific promoter and enhancer elements. As a model, we have tested the effect of oligo length, sequence and number of nuclear factor binding sites on in vitro transcription of adenovirus (Ad) Elb. Short ds oligos containing an SPI-binding sequence (spl) inhibited transcription of Elb by more than 90%. Oligos containing multiple spl sequences were more effective inhibitors than would be expected for a comparable number of unlinked spl sites. A ds oligo with phosphorothioate (PS) linkages inhibited transcription at one-tenth the concentration needed for its normal homologue. An oligo with spl and a consensus TATA site was no more effective than one with spl alone. The stability of the PS-linked oligos will allow testing of this approach in vivo if they are adequately corporated into whole cells.
Url:
DOI: 10.1016/0378-1119(90)90007-E
Affiliations:
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ISTEX:248A69FFF63DB6D77E7515041DCABB88B6823597Le document en format XML
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Jones</name></author><author><name sortKey="Huang, Sheng He" sort="Huang, Sheng He" uniqKey="Huang S" first="Sheng-He" last="Huang">Sheng-He Huang</name></author><author><name sortKey="Calame, Kathryn L" sort="Calame, Kathryn L" uniqKey="Calame K" first="Kathryn L." last="Calame">Kathryn L. 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Holcenberg</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Correspondence to: Dr. J.S. Holcenberg, Division of Hematology-Oncology, Children Hospital of Los Angeles, P.O. Box 54700, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pediatrics, Childrens Hospital of Los Angeles, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Tomich, John" sort="Tomich, John" uniqKey="Tomich J" first="John" last="Tomich">John Tomich</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pediatrics, Childrens Hospital of Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Chen, Jeannie" sort="Chen, Jeannie" uniqKey="Chen J" first="Jeannie" last="Chen">Jeannie Chen</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Jones, Peter A" sort="Jones, Peter A" uniqKey="Jones P" first="Peter A." last="Jones">Peter A. Jones</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Biochemistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Huang, Sheng He" sort="Huang, Sheng He" uniqKey="Huang S" first="Sheng-He" last="Huang">Sheng-He Huang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Pediatrics, Childrens Hospital of Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Calame, Kathryn L" sort="Calame, Kathryn L" uniqKey="Calame K" first="Kathryn L." last="Calame">Kathryn L. Calame</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Department of Microbiology, Columbia College of Physicians and Surgeons, New York</wicri:cityArea></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">89</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="203">203</biblScope><biblScope unit="page" to="209">209</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>Activates transcription</term><term>Antisense oligos</term><term>Aqueous phase</term><term>Assay</term><term>Binding factors</term><term>Binding proteins</term><term>Binding site</term><term>Biosystems user bulletin</term><term>Cancer center</term><term>Childrens hospital</term><term>Complementary overhangs</term><term>Control expression</term><term>Control transcription</term><term>Cooperative interactions</term><term>Enhancer elements</term><term>Functional assay</term><term>Hela cells</term><term>Higher concentrations</term><term>Inhibition</term><term>Inhibitor</term><term>Methylation</term><term>Molar</term><term>Molar ratio</term><term>Molt4 cells</term><term>Nuclear binding factors</term><term>Nuclear extracts</term><term>Nucleic acids</term><term>Oligo</term><term>Oligo length</term><term>Oligos</term><term>Phosphodiester linkage</term><term>Primer</term><term>Primer extension</term><term>Promoter</term><term>Schmidt</term><term>Specific genes</term><term>Splx2b</term><term>Tata</term><term>Therapeutic approach</term><term>Tjian</term><term>Transcription</term><term>Transcriptional</term><term>Transcriptional factor</term><term>Transcriptional unit</term><term>Tris buffer</term><term>Unique factors</term><term>Upper strand</term><term>Whole cells</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: A potential new therapeutic approach to control gene expression is the use of double-stranded (ds) oligodeoxyribonucleotides (oligos) to compete for the binding of nuclear factors to specific promoter and enhancer elements. As a model, we have tested the effect of oligo length, sequence and number of nuclear factor binding sites on in vitro transcription of adenovirus (Ad) Elb. Short ds oligos containing an SPI-binding sequence (spl) inhibited transcription of Elb by more than 90%. Oligos containing multiple spl sequences were more effective inhibitors than would be expected for a comparable number of unlinked spl sites. A ds oligo with phosphorothioate (PS) linkages inhibited transcription at one-tenth the concentration needed for its normal homologue. An oligo with spl and a consensus TATA site was no more effective than one with spl alone. The stability of the PS-linked oligos will allow testing of this approach in vivo if they are adequately corporated into whole cells.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Wu, Henry" sort="Wu, Henry" uniqKey="Wu H" first="Henry" last="Wu">Henry Wu</name></region><name sortKey="Calame, Kathryn L" sort="Calame, Kathryn L" uniqKey="Calame K" first="Kathryn L." last="Calame">Kathryn L. Calame</name><name sortKey="Chen, Jeannie" sort="Chen, Jeannie" uniqKey="Chen J" first="Jeannie" last="Chen">Jeannie Chen</name><name sortKey="Holcenberg, John S" sort="Holcenberg, John S" uniqKey="Holcenberg J" first="John S." last="Holcenberg">John S. Holcenberg</name><name sortKey="Holcenberg, John S" sort="Holcenberg, John S" uniqKey="Holcenberg J" first="John S." last="Holcenberg">John S. Holcenberg</name><name sortKey="Holcenberg, John S" sort="Holcenberg, John S" uniqKey="Holcenberg J" first="John S." last="Holcenberg">John S. Holcenberg</name><name sortKey="Huang, Sheng He" sort="Huang, Sheng He" uniqKey="Huang S" first="Sheng-He" last="Huang">Sheng-He Huang</name><name sortKey="Jones, Peter A" sort="Jones, Peter A" uniqKey="Jones P" first="Peter A." last="Jones">Peter A. Jones</name><name sortKey="Tomich, John" sort="Tomich, John" uniqKey="Tomich J" first="John" last="Tomich">John Tomich</name><name sortKey="Wu, Henry" sort="Wu, Henry" uniqKey="Wu H" first="Henry" last="Wu">Henry Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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