C-rel activates but v-rel suppresses transcription from κB sites

Abstract

We show that the product of the protooncogene c-rel is a constituent of an NF-κB-like complex that binds to the κB site originally identified in the enhancer of immunoglobulin κ light chain gene, c-rel protein synthesized in bacteria binds to the KB site in a sequence-specific manner. The rel-κB complex can be disrupted by incubation with anti-rel antibodies. The rel protein can form oligomers. The c-rel protein can activate transcription from promoters containing κB sites; v-rel, on the other hand, suppresses the transcription of genes linked to κB sites. Thus, v-rel may interfere with the normal transcriptional machinery of the cell by acting as a dominant negative mutant.