Functional interference of Sp1 and NF-kappaB through the same DNA binding site

Item Type:	Article
Title:	Functional interference of Sp1 and NF-kappaB through the same DNA binding site
Creators Name:	Hirano, F. and Tanaka, H. and Hirano, Y. and Hiramoto, M. and Handa, H. and Makino, I. and Scheidereit, C.
Abstract:	Gene activation by NF-kappaB/Rel transcription factors is modulated by synergistic or antagonistic interactions with other promoter-bound transcription factors. For example, Sp1 sites are often found in NF-kappaB-regulated genes, and Sp1 can activate certain promoters in synergism with NF-kappaB through nonoverlapping binding sites. Here we report that Sp1 acts directly through a subset of NF-kappaB binding sites. The DNA binding affinity of Sp1 to these NF-kappaB sites, as determined by their relative dissociation constants and their relative efficiencies as competitor DNAs or as binding site probes, is in the order of that for a consensus GC box Sp1 site. In contrast, NF-kappaB does not bind to a GC box Sp1 site. Sp1 can activate transcription through immunoglobulin kappa-chain enhancer or P-selectin promoter NF-kappaB sites. p50 homodimers replace Sp1 from the P-selectin promoter by binding site competition and thereby either inhibit basal Sp1-driven expression or, in concert with Bcl-3, stimulate expression. The interaction of Sp1 with NF-kappaB sites thus provides a means to keep an elevated basal expression of NF-kappaB-dependent genes in the absence of activated nuclear NF-kappaB/Rel.
Keywords:	Binding Sites, Cell Line, Consensus Sequence, DNA, Genetic Promoter Regions, HeLa Cells, NF-kappa B, NF-kappa B p50 Subunit, Oligodeoxyribonucleotides, Sp1 Transcription Factor, Transcription Factor RelA, Transcriptional Activation, Animals, Drosophila
Source:	Molecular and Cellular Biology
ISSN:	0270-7306
Publisher:	American Society for Microbiology
Volume:	18
Number:	3
Page Range:	1266-1274
Date:	March 1998
Official Publication:	http://mcb.asm.org/cgi/content/abstract/18/3/1266
PubMed:	View item in PubMed

Repository Staff Only: item control page