Abstract
p53-mediated apoptosis of cells with DNA damage or oncogene overexpression is a major mechanism for its function as a tumor suppressor. Both transcriptionally dependent and transcriptionally independent activities of p53 can play a role in mediating cell death. It appears that p53 can induce apoptosis by multiple pathways in a manner which is regulated in a cell type and signal-specific fashion. Understanding the biochemical mechanisms of p53-dependent apoptosis holds a promise of manipulating these pathways in cancer therapy.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis / genetics*
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Caspases / metabolism
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Gene Expression Regulation
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HLA-DR5 Antigen / genetics
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HLA-DR5 Antigen / metabolism
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Humans
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Insulin-Like Growth Factor Binding Protein 3 / genetics
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Insulin-Like Growth Factor Binding Protein 3 / metabolism
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Neoplasms / pathology
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Neoplasms / therapy*
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-bcl-2*
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Transcription, Genetic
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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*
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bcl-2-Associated X Protein
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fas Receptor / genetics
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fas Receptor / metabolism
Substances
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DNA-Binding Proteins
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HLA-DR5 Antigen
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Insulin-Like Growth Factor Binding Protein 3
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Nuclear Proteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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fas Receptor
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Caspases