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- Title
Requirement of NF-kappaB activation to suppress p53-independent apoptosis induced by oncogenic Ras.
- Authors
Mayo, M W; Wang, C Y; Cogswell, P C; Rogers-Graham, K S; Lowe, S W; Der, C J; Baldwin, A S, Jr
- Abstract
The ras proto-oncogene is frequently mutated in human tumors and functions to chronically stimulate signal transduction cascades resulting in the synthesis or activation of specific transcription factors, including Ets, c-Myc, c-Jun, and nuclear factor kappa B (NF-kappaB). These Ras-responsive transcription factors are required for transformation, but the mechanisms by which these proteins facilitate oncogenesis have not been fully established. Oncogenic Ras was shown to initiate a p53-independent apoptotic response that was suppressed through the activation of NF-kappaB. These results provide an explanation for the requirement of NF-kappaB for Ras-mediated oncogenesis and provide evidence that Ras-transformed cells are susceptible to apoptosis even if they do not express the p53 tumor-suppressor gene product.
- Publication
Science (New York, N.Y.), 1997, Vol 278, Issue 5344, p1812
- ISSN
0036-8075
- Publication type
Journal Article
- DOI
10.1126/science.278.5344.1812