Reference : The candidate oncoprotein Bcl-3 is an antagonist of p50/NF-kappa B-mediated inhibition.
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
The candidate oncoprotein Bcl-3 is an antagonist of p50/NF-kappa B-mediated inhibition.
Franzoso, G. [> > > >]
Bours, Vincent mailto [Université de Liège - ULiège > Département des sciences biomédicales et précliniques > GIGA-R : Génétique humaine >]
Park, S. [> > > >]
Tomita-Yamaguchi, M. [> > > >]
Kelly, K. [> > > >]
Siebenlist, U. [> > > >]
Nature Publishing Group
Yes (verified by ORBi)
United Kingdom
[en] Animals ; Ankyrins/genetics ; Cell Line ; Cell Nucleus/metabolism ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Gene Expression ; Glutathione Transferase/genetics/metabolism ; HIV/genetics ; HIV Long Terminal Repeat ; Humans ; NF-kappa B/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Repetitive Sequences, Nucleic Acid ; T-Lymphocytes/metabolism ; Transcription Factors ; Transcription, Genetic ; Transcriptional Activation ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
[en] The candidate oncogene bcl-3 was discovered as a translocation into the immunoglobulin alpha-locus in some cases of B-cell chronic lymphocytic leukaemias. The protein Bcl-3 contains seven so-called ankyrin repeats. Similar repeat motifs are found in a number of diverse regulatory proteins but the motifs of Bcl-3 are most closely related to those found in I kappa B proteins in which the ankyrin repeat domain is thought to be directly involved in inhibition of NF-kappa B activity. No biological function has yet been described for Bcl-3, but it was noted recently that Bcl-3 interferes with DNA-binding of the p50 subunit of NF-kappa B in vitro. Here we demonstrate that Bcl-3 can aid kappa B site-dependent transcription in vivo by counteracting the inhibitory effects of p50/NF-kappa B homodimers. Bcl-3 may therefore aid activation of select NF-kappa B-regulated genes, including those of the human immunodeficiency virus.

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