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REV1 and DNA polymerase zeta in DNA interstrand crosslink repair

dc.contributor.authorSharma, Shilpyen_US
dc.contributor.authorCanman, Christine E.en_US
dc.date.accessioned2012-12-11T17:37:30Z
dc.date.available2014-02-03T16:21:45Zen_US
dc.date.issued2012-12en_US
dc.identifier.citationSharma, Shilpy; Canman, Christine E. (2012). "REV1 and DNA polymerase zeta in DNA interstrand crosslink repair." Environmental and Molecular Mutagenesis 53(9): 725-740. <http://hdl.handle.net/2027.42/94500>en_US
dc.identifier.issn0893-6692en_US
dc.identifier.issn1098-2280en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/94500
dc.description.abstractDNA interstrand crosslinks (ICLs) are covalent linkages between two strands of DNA, and their presence interferes with essential metabolic processes such as transcription and replication. These lesions are extremely toxic, and their repair is essential for genome stability and cell survival. In this review, we will discuss how the removal of ICLs requires interplay between multiple genome maintenance pathways and can occur in the absence of replication (replication‐independent ICL repair) or during S phase (replication‐coupled ICL repair), the latter being the predominant pathway used in mammalian cells. It is now well recognized that translesion DNA synthesis (TLS), especially through the activities of REV1 and DNA polymerase zeta (Polζ), is necessary for both ICL repair pathways operating throughout the cell cycle. Recent studies suggest that the convergence of two replication forks upon an ICL initiates a cascade of events including unhooking of the lesion through the actions of structure‐specific endonucleases, thereby creating a DNA double‐stranded break (DSB). TLS across the unhooked lesion is necessary for restoring the sister chromatid before homologous recombination repair. Biochemical and genetic studies implicate REV1 and Polζ as being essential for performing lesion bypass across the unhooked crosslink, and this step appears to be important for subsequent events to repair the intermediate DSB. The potential role of Fanconi anemia pathway in the regulation of REV1 and Polζ‐dependent TLS and the involvement of additional polymerases, including DNA polymerases kappa, nu, and theta, in the repair of ICLs is also discussed in this review. Environ. Mol. Mutagen. 2012. © 2012 Wiley Periodicals, Inc.en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherRepairen_US
dc.subject.otherFanconi Anemiaen_US
dc.subject.otherTranslesion DNA Synthesisen_US
dc.subject.otherREV1en_US
dc.subject.otherREV3en_US
dc.subject.otherREV7en_US
dc.subject.otherInterstrand Cross Linken_US
dc.titleREV1 and DNA polymerase zeta in DNA interstrand crosslink repairen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelBiological Chemistryen_US
dc.subject.hlbsecondlevelGeneticsen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartment of Pharmacology, University of Michigan Medical School, Biomedical Science Research Building, 109 Zina Pitcher Place, Room 2069, Ann Arbor, MI 48109‐2200, USAen_US
dc.identifier.pmid23065650en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/94500/1/21736_ftp.pdf
dc.identifier.doi10.1002/em.21736en_US
dc.identifier.sourceEnvironmental and Molecular Mutagenesisen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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