Abstract
The specific DNA binding activity of p53 is crucial for its tumor suppression function. Naturally occurring mutant forms of p53 are deficient for specific DNA binding. However, several studies have indicated that their specific DNA binding can be reactivated. Short peptides derived from the p53 C-terminus can reactivate at least some mutant p53 proteins and trigger a p53-dependent biological response. These results may provide the basis for the design of p53-reactivating anti-cancer drugs.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal / therapeutic use
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Genes, p53*
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Humans
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Models, Biological
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Mutation / genetics*
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Neoplasms / drug therapy*
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Neoplasms / genetics
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Peptide Fragments / pharmacology
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Peptide Fragments / therapeutic use
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Suppression, Genetic / genetics
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / physiology*
Substances
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Antibodies, Monoclonal
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Antineoplastic Agents
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Peptide Fragments
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Tumor Suppressor Protein p53