The v-Rel oncoprotein increases expression from Sp1 site-containing promoters in chicken embryo fibroblasts

S. Sif, J. Capobianco, T. D. Gilmore

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

The v-Rel oncoprotein of the avian Rev-T retrovirus is a member of a family of related transcription factors, which also includes the subunits of NF-κB and several other interacting cellular proteins. We show here that v-Rel specifically increased expression from a reporter plasmid containing multiple Sp1 binding sites approximately sixfold in chicken embryo fibroblasts (CEFs), even though v-Rel did not bind directly to these sites. v-Rel also increased expression from a reporter plasmid containing a human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in which the κB binding sites were mutated but which still contained intact Sp1 binding sites. The increase in Sp1-site transactivation does not precisely correlate with transformation by v-Rel since one non-transforming v-Rel mutant still induced expression from the Sp1 site-containing promoter. v-Rel appears to increase expression from Sp1 site-containing promoters by affecting the transactivation domain of Sp1, since v-Rel increased the activity of a Gal4-Sp1 fusion protein, which contains the Sp1 transactivation domain but lacks the Sp1 DNA-binding domain. As compared with v-Rel, c-Rel induced only a slight increase in expression from the reporter plasmid containing Sp1 sites. However, v-Ras and v-Src (but not v-Myb) induced increases in transcription from the reporter plasmid containing Sp1 sites to the same extent as v-Rel, but through pathways that appear to be independent from v-Rel. These results suggest that certain oncoproteins might increase transcription from many genes that contain Sp1 binding sites, and that this might be important for certain aspects of transformation by these proteins.

Original languageEnglish (US)
Pages (from-to)2501-2509
Number of pages9
JournalOncogene
Volume8
Issue number9
StatePublished - Jan 1 1993
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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