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dc.contributor.authorIyer, Divya Ramalingam
dc.contributor.authorRhind, Nicholas R.
dc.date2022-08-11T08:09:47.000
dc.date.accessioned2022-08-23T16:43:25Z
dc.date.available2022-08-23T16:43:25Z
dc.date.issued2017-02-17
dc.date.submitted2017-06-16
dc.identifier.citationGenes (Basel). 2017 Feb 17;8(2). pii: E74. doi: 10.3390/genes8020074. <a href="https://doi.org/10.3390/genes8020074">Link to article on publisher's site</a>
dc.identifier.issn2073-4425 (Linking)
dc.identifier.doi10.3390/genes8020074
dc.identifier.pmid28218681
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40291
dc.description.abstractFaithful duplication of the genome is a challenge because DNA is susceptible to damage by a number of intrinsic and extrinsic genotoxins, such as free radicals and UV light. Cells activate the intra-S checkpoint in response to damage during S phase to protect genomic integrity and ensure replication fidelity. The checkpoint prevents genomic instability mainly by regulating origin firing, fork progression, and transcription of G1/S genes in response to DNA damage. Several studies hint that regulation of forks is perhaps the most critical function of the intra-S checkpoint. However, the exact role of the checkpoint at replication forks has remained elusive and controversial. Is the checkpoint required for fork stability, or fork restart, or to prevent fork reversal or fork collapse, or activate repair at replication forks? What are the factors that the checkpoint targets at stalled replication forks? In this review, we will discuss the various pathways activated by the intra-S checkpoint in response to damage to prevent genomic instability.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28218681&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright © 2017 by the authors.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectATR
dc.subjectChk1
dc.subjectDNA damage
dc.subjectfork stability
dc.subjectintra-S checkpoint
dc.subjectorigin regulation
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectGenetics
dc.subjectMolecular Biology
dc.titleThe Intra-S Checkpoint Responses to DNA Damage
dc.typeJournal Article
dc.source.journaltitleGenes
dc.source.volume8
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4096&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3091
dc.identifier.contextkey10314722
refterms.dateFOA2022-08-23T16:43:25Z
html.description.abstract<p>Faithful duplication of the genome is a challenge because DNA is susceptible to damage by a number of intrinsic and extrinsic genotoxins, such as free radicals and UV light. Cells activate the intra-S checkpoint in response to damage during S phase to protect genomic integrity and ensure replication fidelity. The checkpoint prevents genomic instability mainly by regulating origin firing, fork progression, and transcription of G1/S genes in response to DNA damage. Several studies hint that regulation of forks is perhaps the most critical function of the intra-S checkpoint. However, the exact role of the checkpoint at replication forks has remained elusive and controversial. Is the checkpoint required for fork stability, or fork restart, or to prevent fork reversal or fork collapse, or activate repair at replication forks? What are the factors that the checkpoint targets at stalled replication forks? In this review, we will discuss the various pathways activated by the intra-S checkpoint in response to damage to prevent genomic instability.</p>
dc.identifier.submissionpathoapubs/3091
dc.contributor.departmentGraduate School of Biomedical Sciences, Interdisciplinary Graduate Program
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology


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Copyright © 2017 by the authors.
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