Journal
GENES & DEVELOPMENT
Volume 26, Issue 13, Pages 1393-1408Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.195248.112
Keywords
Fanconi anemia; ubiquitination; DNA interstrand cross-link; DNA repair; translesion DNA synthesis; homologous recombination
Categories
Funding
- Leukemia and Lymphoma Society Career Development Fellowship
- NIH [R01DK43889, R01HL52725, 2P01HL048546]
Ask authors/readers for more resources
The maintenance of genome stability is critical for survival, and its failure is often associated with tumorigenesis. The Fanconi anemia (FA) pathway is essential for the repair of DNA interstrand cross-links (ICLs), and a germline defect in the pathway results in FA, a cancer predisposition syndrome driven by genome instability. Central to this pathway is the monoubiquitination of FANCD2, which coordinates multiple DNA repair activities required for the resolution of ICLs. Recent studies have demonstrated how the FA pathway coordinates three critical DNA repair processes, including nucleolytic incision, translesion DNA synthesis (TLS), and homologous recombination (HR). Here, we review recent advances in our understanding of the downstream ICL repair steps initiated by ubiquitin-mediated FA pathway activation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available