Vernersson-Lindahl, E., Mills, A. A. (March 2010) ΔNp73β puts the brakes on DNA repair. Genes Dev, 24 (6). pp. 517-20. ISSN 1549-5477 (Electronic) 0890-9369 (Linking)
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Abstract
Mammalian cells are barraged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million genomic lesions per cell per day. Networks of proteins that repair these lesions are essential for genome maintenance, and a compromise in these pathways propagates mutations that can cause aging and cancer. The p53 tumor suppressor plays a central role in repairing the effects of DNA damage, and has therefore earned the title of "guardian of the genome." In this issue of Genes & Development, Wilhelm and colleagues (pp. 549-560) demonstrate that p73-an older sibling of p53-inhibits pathways that resolve DNA double-strand breaks.
Item Type: | Paper |
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Uncontrolled Keywords: | DNA repair pathways aging cancer p53 tumor Suppressor DNA damage DNA double-strand breaks |
Subjects: | diseases & disorders > cancer organism description > animal > mammal bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > mutations |
CSHL Authors: | |
Communities: | CSHL labs > Mills lab |
Depositing User: | CSHL Librarian |
Date: | 15 March 2010 |
Date Deposited: | 20 Oct 2011 14:27 |
Last Modified: | 02 Feb 2017 17:00 |
PMCID: | PMC2841329 |
Related URLs: | |
URI: | https://repository.cshl.edu/id/eprint/15577 |
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