Document Detail


Outcomes of p53 activation--spoilt for choice.
MedLine Citation:
PMID:  17158908     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The p53 tumour suppressor protein can efficiently inhibit tumour development. This activity reflects its ability to induce a number of different responses, including cell cycle arrest and apoptosis. Recent studies have revealed some interesting insights into how the choice of response to p53 is regulated, highlighting a correlation between the activation of cell cycle arrest and survival with the ability of p53 to reduce oxidative stress and protect cells from genotoxic damage. Understanding the molecular mechanisms that determine which response is selected may allow us to modulate these pathways so that therapeutic reactivation of p53 favours apoptotic cell death in tumour cells, but a reversible--and therefore far less toxic--induction of cell cycle arrest in normal cells.
Authors:
Karen H Vousden
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of cell science     Volume:  119     ISSN:  0021-9533     ISO Abbreviation:  J. Cell. Sci.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-04-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0052457     Medline TA:  J Cell Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  5015-20     Citation Subset:  IM    
Affiliation:
Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / genetics,  physiology*
Cell Cycle / genetics,  physiology
Humans
Male
Models, Biological
Tumor Suppressor Protein p53 / genetics,  metabolism,  physiology*
Chemical
Reg. No./Substance:
0/Tumor Suppressor Protein p53

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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