Abstract
With nuclear factor-kappaB (NF-kappaB) and p53 functions generally having disparate outcomes for cell survival and cell division, understanding how these pathways are coordinated following a common activation signal such as DNA damage has important implications for cancer therapy. Conflicting reports concerning NF-kappaB and p53 interplay in different cell line models prompted a reexamination of this issue using mouse primary thymocytes and embryonic fibroblasts, plus fibroblasts transformed by E1A12S. Here, we report that following the treatment of these cells with a range of stress stimuli, p53 and NF-kappaB were found to regulate cell cycling and survival independently.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / radiation effects
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Cell Cycle / drug effects
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Cell Cycle / radiation effects
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Cell Line, Transformed
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DNA Damage*
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Doxorubicin / pharmacology
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Embryo, Mammalian / cytology
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Fibroblasts / drug effects*
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Fibroblasts / metabolism*
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Fibroblasts / pathology
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Fibroblasts / radiation effects
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Mice
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Mutagens / toxicity*
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NF-kappa B / metabolism*
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Radiation, Ionizing
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Signal Transduction / drug effects
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T-Lymphocytes / cytology
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T-Lymphocytes / drug effects
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T-Lymphocytes / metabolism
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T-Lymphocytes / radiation effects
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Transcription Factor RelA / metabolism
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Tumor Suppressor Protein p53 / deficiency
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Mutagens
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NF-kappa B
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Transcription Factor RelA
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Tumor Suppressor Protein p53
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Doxorubicin