Targeting of the Sp1 binding sites of HIV-1 long terminal repeat with chromomycin - Disruption of nuclear factor center dot DNA complexes and inhibition of in vitro transcription

被引:40
作者
Bianchi, N [1 ]
Passadore, M [1 ]
Rutigliano, C [1 ]
Feriotto, G [1 ]
Mischiati, C [1 ]
Gambari, R [1 ]
机构
[1] UNIV FERRARA,CTR BIOTECHNOL,I-44100 FERRARA,ITALY
关键词
DNA-binding drugs; HIV-1; chromomycin; transcription factors; DNase I footprinting in vitro transcription;
D O I
10.1016/S0006-2952(96)00510-2
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 Spl. Accordingly, interactions between nuclear proteins and Spl binding sites are inhibited by chromomycin, and this effect leads to a sharp inhibition of in vitro transcription. Copyright (C) 1996 Elsevier Science Inc.
引用
收藏
页码:1489 / 1498
页数:10
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