Mechanism and regulation of incisions during DNA interstrand cross-link repair.
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.
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, United States.
Jieqiong
J
Zhang
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.
Johannes C
JC
Walter
D004249:DNA Damage / Q000235:genetics*; D004260:DNA Repair / Q000235:genetics*; D004261:DNA Replication / Q000235:genetics*; D004277:DNA, Single-Stranded / Q000235:genetics* / Q000378:metabolism; D052236:Fanconi Anemia Complementation Group D2 Protein / Q000235:genetics / Q000378:metabolism; D006801:Humans; D045522:Recombinases / Q000235:genetics / Q000378:metabolism
D004277:DNA, Single-Stranded; C499905:FANCD2 protein, human; D052236:Fanconi Anemia Complementation Group D2 Protein; D045522:Recombinases
DNA interstrand crosslink repair; EME1; ERCC1; FAN1; FANCD2; FANCI; Fanconi anemia; MUS81; SLX1; SLX4; SNM1A; XPF