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.
Biochem Pharmacol
; 52(10): 1489-98, 1996 Nov 22.
Article
en En
| MEDLINE
| ID: mdl-8937462
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.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Cromomicinas
/
Duplicado del Terminal Largo de VIH
/
Factor de Transcripción Sp1
/
VIH-1
/
Inhibidores de la Síntesis del Ácido Nucleico
Límite:
Humans
Idioma:
En
Revista:
Biochem Pharmacol
Año:
1996
Tipo del documento:
Article
País de afiliación:
Italia
Pais de publicación:
Reino Unido