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DC Field | Value | Language |
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dc.citation.endPage | 1944 | - |
dc.citation.number | 24 | - |
dc.citation.startPage | 1934 | - |
dc.citation.title | CURRENT BIOLOGY | - |
dc.citation.volume | 11 | - |
dc.contributor.author | Ahmed, S | - |
dc.contributor.author | Alpi, A | - |
dc.contributor.author | Hengartner, MO | - |
dc.contributor.author | Gartner, A | - |
dc.date.accessioned | 2023-12-22T11:40:53Z | - |
dc.date.available | 2023-12-22T11:40:53Z | - |
dc.date.created | 2020-01-30 | - |
dc.date.issued | 2001-12 | - |
dc.description.abstract | Background: In response to genotoxic stress, cells activate checkpoint pathways that lead to a transient cell cycle arrest that allows for DNA repair or to apoptosis, which triggers the demise of genetically damaged cells. Results: During positional cloning of the C. elegans rad-5 DNA damage checkpoint gene, we found, surprisingly, that rad-5(mn159) is allelic with clk-2(qm37), a mutant previously implicated in regulation of biological rhythms and life span. However, clk-2(qm37) is the only C. elegans clock mutant that is defective for the DNA damage checkpoint. We show that rad-5/clk-2 acts in a pathway that partially overlaps with the conserved C. elegans mrt-2/S. cerevisiae RAD17/S. pombe rad1 (+) checkpoint pathway. In addition, rad-5/clk-2 also regulates the S phase replication checkpoint in C. elegans. Positional cloning reveals that the RAD-5/CLK-2 DNA damage checkpoint protein is homologous to S, cerevisiae Tel2p, an essential DNA binding protein that regulates telomere length in, yeast. However, the partial loss-of-function C. elegans rad-5(mn 159) and clk-2(qm37) checkpoint mutations have little effect on telomere length, and analysis of the partial loss-of-function of S. cerevisiae tel2-1 mutant failed to reveal typical DNA damage checkpoint defects. Conclusions: Using C. elegans genetics we define the novel DNA damage checkpoint protein RAD-5/CLK-2, which may play a role in oncogenesis. Given that Tel2p has been shown to bind to a variety of nucleic, acid structures in vitro, we speculate that the RAD-5/CLK-2 checkpoint protein may act at sites of DNA damage, either as a sensor of DNA damage or to aid in the repair of damaged DNA. | - |
dc.identifier.bibliographicCitation | CURRENT BIOLOGY, v.11, no.24, pp.1934 - 1944 | - |
dc.identifier.doi | 10.1016/S0960-9822(01)00604-2 | - |
dc.identifier.issn | 0960-9822 | - |
dc.identifier.scopusid | 2-s2.0-0035846599 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/30922 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0960982201006042?via%3Dihub | - |
dc.identifier.wosid | 000172754700021 | - |
dc.language | 영어 | - |
dc.publisher | CELL PRESS | - |
dc.title | C-elegans RAD-5/CLK-2 defines a new DNA damage checkpoint protein | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology; Biology; Cell Biology | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | REPLICATION-FACTOR-C | - |
dc.subject.keywordPlus | SACCHAROMYCES-CEREVISIAE | - |
dc.subject.keywordPlus | CAENORHABDITIS-ELEGANS | - |
dc.subject.keywordPlus | TELOMERE LENGTH | - |
dc.subject.keywordPlus | CELL-CYCLE | - |
dc.subject.keywordPlus | SCHIZOSACCHAROMYCES-POMBE | - |
dc.subject.keywordPlus | ATAXIA-TELANGIECTASIA | - |
dc.subject.keywordPlus | GENOMIC ANALYSIS | - |
dc.subject.keywordPlus | COMPLEX | - |
dc.subject.keywordPlus | GENES | - |
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