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DNA Repair (Amst). 2014 Jul;19:135-42. doi: 10.1016/j.dnarep.2014.03.018. Epub 2014 Apr 24.

Mechanism and regulation of incisions during DNA interstrand cross-link repair.

Author information

1
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, United States.
2
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, United States; Howard Hughes Medical Institute. Electronic address: johannes_walter@hms.harvard.edu.

Abstract

A critical step in DNA interstrand cross-link repair is the programmed collapse of replication forks that have stalled at an ICL. This event is regulated by the Fanconi anemia pathway, which suppresses bone marrow failure and cancer. In this perspective, we focus on the structure of forks that have stalled at ICLs, how these structures might be incised by endonucleases, and how incision is regulated by the Fanconi anemia pathway.

KEYWORDS:

DNA interstrand crosslink repair; EME1; ERCC1; FAN1; FANCD2; FANCI; Fanconi anemia; MUS81; SLX1; SLX4; SNM1A; XPF

PMID:
24768452
PMCID:
PMC4076290
DOI:
10.1016/j.dnarep.2014.03.018
[Indexed for MEDLINE]
Free PMC Article
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