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Links between mutant p53 and genomic instability

✍ Scribed by Walter Hanel; Ute M. Moll


Book ID
102301225
Publisher
John Wiley and Sons
Year
2012
Tongue
English
Weight
325 KB
Volume
113
Category
Article
ISSN
0730-2312

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✦ Synopsis


Abstract

The tumor suppressor p53 has long been known to play a central role in maintaining a stable genome in the face of toxic insults through its role in promoting cell‐cycle checkpoints, DNA repair, and apoptosis. However, p53 null cells still retain some function of certain checkpoint and repair processes, reducing the genomic changes that otherwise would occur if these mechanisms were absent. Accumulating evidence suggests that mutant forms of p53 proteins may drastically perturb these residual genome‐stabilizing mechanisms through gain‐of‐function interactions with multiple proteins leading to a higher level of genomic instability than in p53 null cells. This review summarizes the current body of evidence that mutp53 plays a role in promoting various forms of genomic instability and provides an overview of current mechanistic proposals. J. Cell. Biochem. 113: 433–439, 2012. Β© 2011 Wiley Periodicals, Inc.


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