Journal
SCIENCE
Volume 329, Issue 5992, Pages 693-696Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1192656
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Funding
- Life Sciences Institute, Zhejiang University
- Fundamental Research Funds for the Central Universities, China
- NIH
- U.S. Department of Defense
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Fanconi anemia (FA) is caused by mutations in 13 Fanc genes and renders cells hypersensitive to DNA interstrand cross-linking (ICL) agents. A central event in the FA pathway is mono-ubiquitylation of the FANCI-FANCD2 (ID) protein complex. Here, we characterize a previously unrecognized nuclease, Fanconi anemia-associated nuclease 1 (FAN1), that promotes ICL repair in a manner strictly dependent on its ability to accumulate at or near sites of DNA damage and that relies on mono-ubiquitylation of the ID complex. Thus, the mono-ubiquitylated ID complex recruits the downstream repair protein FAN1 and facilitates the repair of DNA interstrand cross-links.
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