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DC Field | Value | Language |
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dc.citation.number | 1 | - |
dc.citation.title | PLOS GENETICS | - |
dc.citation.volume | 6 | - |
dc.contributor.author | Lee, Se-Jin | - |
dc.contributor.author | Gartner, Anton | - |
dc.contributor.author | Hyun, Moonjung | - |
dc.contributor.author | Ahn, Byungchan | - |
dc.contributor.author | Koo, Hyeon-Sook | - |
dc.date.accessioned | 2023-12-22T07:14:49Z | - |
dc.date.available | 2023-12-22T07:14:49Z | - |
dc.date.created | 2020-01-30 | - |
dc.date.issued | 2010-01 | - |
dc.description.abstract | WRN-1 is the Caenorhabditis elegans homolog of the human Werner syndrome protein, a RecQ helicase, mutations of which are associated with premature aging and increased genome instability. Relatively little is known as to how WRN-1 functions in DNA repair and DNA damage signaling. Here, we take advantage of the genetic and cytological approaches in C. elegans to dissect the epistatic relationship of WRN-1 in various DNA damage checkpoint pathways. We found that WRN-1 is required for CHK1 phosphorylation induced by DNA replication inhibition, but not by UV radiation. Furthermore, WRN-1 influences the RPA-1 focus formation, suggesting that WRN-1 functions in the same step or upstream of RPA-1 in the DNA replication checkpoint pathway. In response to ionizing radiation, RPA-1 focus formation and nuclear localization of ATM depend on WRN-1 and MRE-11. We conclude that C. elegans WRN-1 participates in the initial stages of checkpoint activation induced by DNA replication inhibition and ionizing radiation. These functions of WRN-1 in upstream DNA damage signaling are likely to be conserved, but might be cryptic in human systems due to functional redundancy. | - |
dc.identifier.bibliographicCitation | PLOS GENETICS, v.6, no.1 | - |
dc.identifier.doi | 10.1371/journal.pgen.1000801 | - |
dc.identifier.issn | 1553-7390 | - |
dc.identifier.scopusid | 2-s2.0-76749085278 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/31001 | - |
dc.identifier.url | https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000801 | - |
dc.identifier.wosid | 000274194300009 | - |
dc.language | 영어 | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.title | The Caenorhabditis elegans Werner Syndrome Protein Functions Upstream of ATR and ATM in Response to DNA Replication Inhibition and Double-Strand DNA Breaks | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity | - |
dc.relation.journalResearchArea | Genetics & Heredity | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | EXONUCLEASE | - |
dc.subject.keywordPlus | C-ELEGANS | - |
dc.subject.keywordPlus | DAMAGE CHECKPOINT | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | SYNDROME HELICASE | - |
dc.subject.keywordPlus | RECQ HELICASE | - |
dc.subject.keywordPlus | LIFE-SPAN | - |
dc.subject.keywordPlus | S-PHASE | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
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