Open Accessc-rel activates but v-rel suppresses transcription from kappa B sites.
Author(s) -
Junichiro Inoue,
Lawrence D. Kerr,
Lynn J. Ransone,
Eyal Bengal,
Tony Hunter,
Inder M. Verma
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.9.3715
Subject(s) - enhancer , kappa , transcription (linguistics) , biology , promoter , microbiology and biotechnology , gene , transcription factor , dna binding protein , genetics , gene expression , linguistics , philosophy
We show that the product of the protooncogene c-rel is a constituent of an NF-kappa B-like complex that binds to the kappa B site originally identified in the enhancer of immunoglobulin kappa light chain gene. c-rel protein synthesized in bacteria binds to the kappa B site in a sequence-specific manner. The rel-kappa B 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 kappa B sites; v-rel, on the other hand, suppresses the transcription of genes linked to kappa B sites. Thus, v-rel may interfere with the normal transcriptional machinery of the cell by acting as a dominant negative mutant.