An essential role for NF-kappaB in preventing TNF-alpha-induced cell death
- PMID: 8864118
- DOI: 10.1126/science.274.5288.782
An essential role for NF-kappaB in preventing TNF-alpha-induced cell death
Abstract
Studies on mice deficient in nuclear factor kappa B (NF-kappaB) 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.
Comment in
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Life-death balance within the cell.Science. 1996 Nov 1;274(5288):724. doi: 10.1126/science.274.5288.724. Science. 1996. PMID: 8966553 No abstract available.
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Transcription factors, oncogenes, and apoptosis.Science. 1997 Apr 11;276(5310):185. doi: 10.1126/science.276.5310.181f. Science. 1997. PMID: 9132938 No abstract available.
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