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      An essential role for NF-kappaB in preventing TNF-alpha-induced cell death.

      Science (New York, N.Y.)

      3T3 Cells, Animals, Antigens, CD, metabolism, Cell Death, Cell Survival, Cells, Cultured, Gene Expression Regulation, Humans, Macrophages, cytology, Mice, NF-kappa B, genetics, physiology, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Type I, Signal Transduction, Transcription Factor RelA, Transfection, Tumor Necrosis Factor-alpha, pharmacology

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          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.

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          8864118

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