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Science 1 November 1996:
Vol. 274. no. 5288, pp. 782 - 784
DOI: 10.1126/science.274.5288.782
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Reports

An Essential Role for NF-kappa B in Preventing TNF-alpha -Induced Cell Death

Amer A. Beg * and David Baltimore dagger

Studies on mice deficient in nuclear factor kappa B (NF-kappa B) subunits have shown that this transcription factor is important for lymphocyte responses to antigens and cytokine-inducible gene expression. In particular, the RelA (p65) subunit is required for induction of tumor necrosis factor-alpha (TNF-alpha )-dependent genes. Treatment of RelA-deficient (RelA-/-) mouse fibroblasts and macrophages with TNF-alpha resulted in a significant reduction in viability, whereas RelA+/+ cells were unaffected. Cytotoxicity to both cell types was mediated by TNF receptor 1. Reintroduction of RelA into RelA-/- fibroblasts resulted in enhanced survival, demonstrating that the presence of RelA is required for protection from TNF-alpha . These results have implications for the treatment of inflammatory and proliferative diseases.

Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
*   Present address: Department of Biological Sciences, Columbia University, New York, NY 10027, USA.

dagger    To whom correspondence should be addressed.

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Science. ISSN 0036-8075 (print), 1095-9203 (online)