Abstract
Since the initial concept of p53 as a sensor of DNA-damage, the picture of the role of p53 has widened to include the sensing of much more diverse forms of stress, including hypoxia and constitutive activation of growth-promoting cascades. The pathways by which these processes regulate p53 are partially overlapping, but imply different patterns of post-translational modifications. In this review, we summarize current knowledge on post-translational modifications of p53, and we discuss how hypoxia and oncogene activation stresses may induce p53 independently of DNA damage.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Apoptosis
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Cell Cycle
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Cell Hypoxia
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DNA Damage
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Gene Expression Regulation, Neoplastic
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Humans
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases / metabolism
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Mutagens / metabolism*
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Nuclear Proteins*
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Oncogenes / genetics
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Protein Processing, Post-Translational
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-mdm2
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Signal Transduction*
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Tumor Suppressor Protein p53 / chemistry
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Mutagens
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Nuclear Proteins
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Proto-Oncogene Proteins
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Tumor Suppressor Protein p53
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MDM2 protein, human
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Proto-Oncogene Proteins c-mdm2
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases