Open Access
CC BY 4.0 · AIMS Genet 2018; 05(04): 192-211
DOI: 10.3934/genet.2018.4.192
Review

Homologous recombination defects and how they affect replication fork maintenance

Mi Young Son
1   Department of Molecular Medicine and Institute of Biotechnology, UT Health San Antonio, 15355 Lambda Drive, San Antonio, USA
,
Paul Hasty
1   Department of Molecular Medicine and Institute of Biotechnology, UT Health San Antonio, 15355 Lambda Drive, San Antonio, USA
2   The Mays Cancer Center, USA
3   Sam and Ann Barshop Institute for Longevity and Aging Studies, USA
› Institutsangaben
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Abstract

Homologous recombination (HR) repairs DNA double strand breaks (DSBs) and stabilizes replication forks (RFs). RAD51 is the recombinase for the HR pathway. To preserve genomic integrity, RAD51 forms a filament on the 3″ end of a DSB and on a single-stranded DNA (ssDNA) gap. But unregulated HR results in undesirable chromosomal rearrangements. This review describes the multiple mechanisms that regulate HR with a focus on those mechanisms that promote and contain RAD51 filaments to limit chromosomal rearrangements. If any of these pathways break down and HR becomes unregulated then disease, primarily cancer, can result.



Publikationsverlauf

Eingereicht: 22. Januar 2019

Angenommen: 18. März 2019

Artikel online veröffentlicht:
10. Mai 2021

© 2018. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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