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

来源：

BIOCHEMICAL PHARMACOLOGY | 1996年 / 52卷 / 10期

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

页码：1489 / 1498

页数：10

共 44 条

[41] CHROMOMYCIN, MITHRAMYCIN, AND OLIVOMYCIN BINDING-SITES ON HETEROGENEOUS DEOXYRIBONUCLEIC-ACID - FOOTPRINTING WITH (METHIDIUMPROPYL-EDTA)IRON(II) [J].