| First Author | Beg AA | Year | 1996 |
| Journal | Science | Volume | 274 |
| Issue | 5288 | Pages | 782-4 |
| PubMed ID | 8864118 | Mgi Jnum | J:36492 |
| Mgi Id | MGI:83919 | Doi | 10.1126/science.274.5288.782 |
| Citation | Beg AA, et al. (1996) An essential role for NF-kappaB in preventing TNF-alpha-induced cell death [see comments]. Science 274(5288):782-4 |
| abstractText | 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. |
