Targeting of the Sp1 binding sites of HIV-1 long terminal repeat with chromomycin. Disruption of nuclear factor.DNA complexes and inhibition of in vitro transcription
Sequence selectivity of DNA-binding drugs has recently been reported in a number of studies employing footprinting and gel retardation approaches. In this paper, we studied the biochemical effects of the sequence-selective binding of chromomycin to the long terminal repeat of the human immunodeficie...
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| Veröffentlicht in: | Biochemical pharmacology 1996-11, Vol.52 (10), p.1489-1498 |
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| creator | Bianchi, N Passadore, M Rutigliano, C Feriotto, G Mischiati, C Gambari, R |
| description | Sequence selectivity of DNA-binding drugs has recently been reported in a number of studies employing footprinting and gel retardation approaches. In this paper, we studied the biochemical effects of the sequence-selective binding of chromomycin to the long terminal repeat of the human immunodeficiency type I virus. Deoxyribonuclease I (E.C.3.1.21.1) footprinting, arrested polymerase chain reaction, gel retardation and in vitro transcription experiments have demonstrated that chromomycin preferentially interacts with the binding sites of the promoter-specific transcription factor Sp1. Accordingly, interactions between nuclear proteins and Sp1 binding sites are inhibited by chromomycin, and this effect leads to a sharp inhibition of in vitro transcription. |
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Accordingly, interactions between nuclear proteins and Sp1 binding sites are inhibited by chromomycin, and this effect leads to a sharp inhibition of in vitro transcription.</description><identifier>ISSN: 0006-2952</identifier><identifier>PMID: 8937462</identifier><language>eng</language><publisher>England</publisher><subject>AIDS/HIV ; Base Sequence ; Binding Sites - genetics ; Chromomycins - metabolism ; Chromomycins - pharmacology ; DNA - genetics ; DNA - metabolism ; DNA Footprinting ; DNA Primers - genetics ; HeLa Cells ; HIV Long Terminal Repeat ; HIV-1 - drug effects ; HIV-1 - genetics ; HIV-1 - metabolism ; Humans ; In Vitro Techniques ; Jurkat Cells ; Nuclear Proteins - metabolism ; Nucleic Acid Synthesis Inhibitors - metabolism ; Nucleic Acid Synthesis Inhibitors - pharmacology ; Polymerase Chain Reaction ; Sp1 Transcription Factor - metabolism ; Transcription, Genetic - drug effects</subject><ispartof>Biochemical pharmacology, 1996-11, Vol.52 (10), p.1489-1498</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8937462$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bianchi, N</creatorcontrib><creatorcontrib>Passadore, M</creatorcontrib><creatorcontrib>Rutigliano, C</creatorcontrib><creatorcontrib>Feriotto, G</creatorcontrib><creatorcontrib>Mischiati, C</creatorcontrib><creatorcontrib>Gambari, R</creatorcontrib><title>Targeting of the Sp1 binding sites of HIV-1 long terminal repeat with chromomycin. Disruption of nuclear factor.DNA complexes and inhibition of in vitro transcription</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Sequence selectivity of DNA-binding drugs has recently been reported in a number of studies employing footprinting and gel retardation approaches. In this paper, we studied the biochemical effects of the sequence-selective binding of chromomycin to the long terminal repeat of the human immunodeficiency type I virus. Deoxyribonuclease I (E.C.3.1.21.1) footprinting, arrested polymerase chain reaction, gel retardation and in vitro transcription experiments have demonstrated that chromomycin preferentially interacts with the binding sites of the promoter-specific transcription factor Sp1. Accordingly, interactions between nuclear proteins and Sp1 binding sites are inhibited by chromomycin, and this effect leads to a sharp inhibition of in vitro transcription.</description><subject>AIDS/HIV</subject><subject>Base Sequence</subject><subject>Binding Sites - genetics</subject><subject>Chromomycins - metabolism</subject><subject>Chromomycins - pharmacology</subject><subject>DNA - genetics</subject><subject>DNA - metabolism</subject><subject>DNA Footprinting</subject><subject>DNA Primers - genetics</subject><subject>HeLa Cells</subject><subject>HIV Long Terminal Repeat</subject><subject>HIV-1 - drug effects</subject><subject>HIV-1 - genetics</subject><subject>HIV-1 - metabolism</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Jurkat Cells</subject><subject>Nuclear Proteins - metabolism</subject><subject>Nucleic Acid Synthesis Inhibitors - metabolism</subject><subject>Nucleic Acid Synthesis Inhibitors - pharmacology</subject><subject>Polymerase Chain Reaction</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Transcription, Genetic - drug effects</subject><issn>0006-2952</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kMFOwzAMhnsAjTF4BKScuHVa0rVLjtMGbNIEByaulZOmq1GblCQF9kJ7TloY8sHy79-ffvkiGs9msyxmImVX0bX378PIMzqKRlwki3nGxtFpD-6gA5oDsSUJlSavLSUSTTFIHoP2w2KzfYspqW2vBe0aNFATp1sNgXxhqIiqnG1sc1RopmSN3nVtQGuGU9OpWoMjJahg3XT9vCTKNm2tv3s0mIKgqVDivx0N-cTgLAkOjFcOf0E30WUJtde35z6J9o8P-9Um3r08bVfLXdymCYsTKCiXck5TJhlIrthCUgoyZbwEwUWZalomLOPAUy5oyYUshMrmGad9OkaTSXT_h22d_ei0D3mDXum6BqNt5_MFTzPWV2-8Oxs72egibx024I75-a_JD33Gdfg</recordid><startdate>19961122</startdate><enddate>19961122</enddate><creator>Bianchi, N</creator><creator>Passadore, M</creator><creator>Rutigliano, C</creator><creator>Feriotto, G</creator><creator>Mischiati, C</creator><creator>Gambari, R</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19961122</creationdate><title>Targeting of the Sp1 binding sites of HIV-1 long terminal repeat with chromomycin. 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Disruption of nuclear factor.DNA complexes and inhibition of in vitro transcription</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>1996-11-22</date><risdate>1996</risdate><volume>52</volume><issue>10</issue><spage>1489</spage><epage>1498</epage><pages>1489-1498</pages><issn>0006-2952</issn><abstract>Sequence selectivity of DNA-binding drugs has recently been reported in a number of studies employing footprinting and gel retardation approaches. In this paper, we studied the biochemical effects of the sequence-selective binding of chromomycin to the long terminal repeat of the human immunodeficiency type I virus. Deoxyribonuclease I (E.C.3.1.21.1) footprinting, arrested polymerase chain reaction, gel retardation and in vitro transcription experiments have demonstrated that chromomycin preferentially interacts with the binding sites of the promoter-specific transcription factor Sp1. Accordingly, interactions between nuclear proteins and Sp1 binding sites are inhibited by chromomycin, and this effect leads to a sharp inhibition of in vitro transcription.</abstract><cop>England</cop><pmid>8937462</pmid><tpages>10</tpages></addata></record> |
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| identifier | ISSN: 0006-2952 |
| ispartof | Biochemical pharmacology, 1996-11, Vol.52 (10), p.1489-1498 |
| issn | 0006-2952 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | AIDS/HIV Base Sequence Binding Sites - genetics Chromomycins - metabolism Chromomycins - pharmacology DNA - genetics DNA - metabolism DNA Footprinting DNA Primers - genetics HeLa Cells HIV Long Terminal Repeat HIV-1 - drug effects HIV-1 - genetics HIV-1 - metabolism Humans In Vitro Techniques Jurkat Cells Nuclear Proteins - metabolism Nucleic Acid Synthesis Inhibitors - metabolism Nucleic Acid Synthesis Inhibitors - pharmacology Polymerase Chain Reaction Sp1 Transcription Factor - metabolism Transcription, Genetic - drug effects |
| title | Targeting of the Sp1 binding sites of HIV-1 long terminal repeat with chromomycin. Disruption of nuclear factor.DNA complexes and inhibition of in vitro transcription |
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