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- W3049398524 endingPage "102943" @default.
- W3049398524 startingPage "102943" @default.
- W3049398524 abstract "Over the course of DNA replication, DNA lesions, transcriptional intermediates and protein-DNA complexes can impair the progression of replication forks, thus resulting in replication stress. Failure to maintain replication fork integrity in response to replication stress leads to genomic instability and predisposes to the development of cancer and other genetic disorders. Multiple DNA damage and repair pathways have evolved to allow completion of DNA replication following replication stress, thus preserving genomic integrity. One of the processes commonly induced in response to replication stress is fork reversal, which consists in the remodeling of stalled replication forks into four-way DNA junctions. In normal conditions, fork reversal slows down replication fork progression to ensure accurate repair of DNA lesions and facilitates replication fork restart once the DNA lesions have been removed. However, in certain pathological situations, such as the deficiency of DNA repair factors that protect regressed forks from nuclease-mediated degradation, fork reversal can cause genomic instability. In this review, we describe the complex molecular mechanisms regulating fork reversal, with a focus on the role of the SNF2-family fork remodelers SMARCAL1, ZRANB3 and HLTF, and highlight the implications of fork reversal for tumorigenesis and cancer therapy." @default.
- W3049398524 created "2020-08-21" @default.
- W3049398524 creator A5006411138 @default.
- W3049398524 creator A5024098581 @default.
- W3049398524 creator A5028338080 @default.
- W3049398524 creator A5039060297 @default.
- W3049398524 creator A5042132774 @default.
- W3049398524 creator A5084138562 @default.
- W3049398524 date "2020-11-01" @default.
- W3049398524 modified "2023-10-17" @default.
- W3049398524 title "Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease" @default.
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