| New developments in the multi-site phosphorylation and integration of stress signalling at p53. | |
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MedLine Citation:
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PMID: 9881718 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: To summarize recent progress in the understanding of the role of multi-site phosphorylation in mediating the integration of stress signals at the p53 tumour suppressor protein. RESULTS: The p53 protein plays a key role in the response to a range of cellular stresses including agents that can damage DNA; consequently the involvement of p53 in sensing these effects is central to the prevention of tumour development. p53 is a potent but latent transcription factor that can be activated by a range of cellular stresses leading to the induction of cellular growth arrest or controlled cell removal through apoptosis. Accordingly, p53 is under tight control and is subject to several levels of regulation including multi-site phosphorylation. Recent evidence has implicated individual phosphorylation events in the activation of p53 by different types of stress (e.g. ionizing radiation, UV and mitotic spindle damage). CONCLUSIONS: A picture is now emerging of the p53 protein as an integration point for stress signals. Different signals impinge on different domains of the protein and may cooperate in modulating the type of p53 response, depending on the nature of the incoming signal. |
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Authors:
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D W Meek |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: International journal of radiation biology Volume: 74 ISSN: 0955-3002 ISO Abbreviation: Int. J. Radiat. Biol. Publication Date: 1998 Dec |
Date Detail:
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Created Date: 1999-01-22 Completed Date: 1999-01-22 Revised Date: 2005-11-17 |
Medline Journal Info:
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Nlm Unique ID: 8809243 Medline TA: Int J Radiat Biol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 729-37 Citation Subset: IM; S |
Affiliation:
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Biomedical Research Centre, Ninewells Hospital and Medical School, University of Dundee, UK. meek@icrf.icnet.uk |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Chromosomes
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radiation effects DNA Damage / genetics Mitosis / radiation effects Phosphorylation / radiation effects Ploidies Radiation, Ionizing Signal Transduction / radiation effects* Tumor Suppressor Protein p53 / metabolism* Ultraviolet Rays |
| Chemical | |
Reg. No./Substance:
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0/Tumor Suppressor Protein p53 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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