Journal
EMBO REPORTS
Volume 12, Issue 5, Pages 444-450Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/embor.2011.46
Keywords
APOBEC3A; cytidine deaminase; DNA damage; uracil-DNA glycosylase
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Funding
- Pioneer Developmental Chair from the Salk Institute
- National Institutes of Health [AI067952, AI074967]
- Instituto de Salud 'Carlos III'/Consejo Superior de Investigaciones Cientificas/Salk Institute
- Lynn Streim Postdoctoral Endowment Fellowship
- Natural Sciences & Engineering Research Council of Canada
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Human apolipoprotein-B mRNA-editing catalytic polypeptide-like 3 (APOBEC3) proteins constitute a family of cytidine deaminases that mediate restriction of retroviruses, endogenous retro-elements and DNA viruses. It is well established that these enzymes are potent mutators of viral DNA, but it is unclear whether their editing activity is a threat to the integrity of the cellular genome. We show that expression of APOBEC3A can lead to induction of DNA breaks and activation of damage responses in a deaminase-dependent manner. Consistent with these observations, APOBEC3A expression induces cell-cycle arrest. These results indicate that cellular DNA is vulnerable to APOBEC3 activity and deregulated expression of APOBEC3A could threaten genomic integrity.
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