The involvement of NF-kappa B in beta-interferon gene regulation reveals its role as widely inducible mediator of signal transduction.
The DNA binding protein NF-kappa B has been implicated in gene regulation in B and T lymphocytes. We have found that NF-kappa B also has a central role in virus induction of human beta-interferon (beta-IFN) gene expression. A critical virus-inducible element of this gene, PRDII, behaves interchangeably with the NF-kappa B binding site from the Ig kappa enhancer in both B lymphocytes and virus-infected fibroblasts. Single base substitutions that impair inducibility of the beta-IFN gene in vivo also reduce the binding of NF-kappa B to PRDII in vitro. Virus infection potently activates the binding and nuclear localization of NF-kappa B and, in pre-B lymphocytes, results in the expression of both the beta-IFN gene and the Ig kappa gene. The wide variety of cell types in which beta-interferon can be induced and the divergent set of gene induction processes involving NF-kappa B suggest that this transcription factor plays a broad role in gene regulation as a mediator of inducible signal transduction.[1]References
- The involvement of NF-kappa B in beta-interferon gene regulation reveals its role as widely inducible mediator of signal transduction. Lenardo, M.J., Fan, C.M., Maniatis, T., Baltimore, D. Cell (1989) [Pubmed]
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