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DC Field | Value | Language |
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dc.citation.endPage | 338 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 333 | - |
dc.citation.title | CURRENT BIOLOGY | - |
dc.citation.volume | 20 | - |
dc.contributor.author | Ito, Shu | - |
dc.contributor.author | Greiss, Sebastian | - |
dc.contributor.author | Gartner, Anton | - |
dc.contributor.author | Derry, W. Brent | - |
dc.date.accessioned | 2023-12-22T07:12:48Z | - |
dc.date.available | 2023-12-22T07:12:48Z | - |
dc.date.created | 2020-01-30 | - |
dc.date.issued | 2010-02 | - |
dc.description.abstract | Programmed cell death (or apoptosis) is an evolutionarily conserved, genetically controlled suicide mechanism for cells that, when deregulated, can lead to developmental defects, cancers, and degenerative diseases [1, 2]. In C. elegans, DNA damage induces germ cell death by signaling through cep-1/p53, ultimately leading to the activation of CED-3/caspase [3-13]. It has been hypothesized that the major regulatory events controlling cell death occur by cell-autonomous mechanisms, that is, within the dying cell. In support of this, genetic studies in C. elegans have shown that the core apoptosis pathway genes ced-4l APAF-1 and ced-3/caspase are required in cells fated to die [9]. However, it is not known whether the upstream signals that activate apoptosis function in a cell-autonomous manner. Here we show that kri-1, an ortholog of KRIT1/CCM1, which is mutated in the human neurovascular disease cerebral cavernous malformation [14, 15], is required to activate DNA damage-dependent cell death independently of cep-1/p53. Interestingly, we find that kri-1 regulates cell death in a cell-nonautonomous manner, revealing a novel regulatory role for nondying cells in eliciting cell death in response to DNA damage. | - |
dc.identifier.bibliographicCitation | CURRENT BIOLOGY, v.20, no.4, pp.333 - 338 | - |
dc.identifier.doi | 10.1016/j.cub.2009.12.032 | - |
dc.identifier.issn | 0960-9822 | - |
dc.identifier.scopusid | 2-s2.0-76749108400 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/31000 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0960982209021563?via%3Dihub | - |
dc.identifier.wosid | 000275149200034 | - |
dc.language | 영어 | - |
dc.publisher | CELL PRESS | - |
dc.title | Cell-Nonautonomous Regulation of C. elegans Germ Cell Death by kri-1 | - |
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 | GENE | - |
dc.subject.keywordPlus | CED-4 | - |
dc.subject.keywordPlus | P53 | - |
dc.subject.keywordPlus | DAMAGE-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | CAENORHABDITIS-ELEGANS | - |
dc.subject.keywordPlus | CHECKPOINT PROTEIN | - |
dc.subject.keywordPlus | LIFE-SPAN | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | ENCODING KRIT1 | - |
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