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DC Field | Value | Language |
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dc.citation.endPage | 879 | - |
dc.citation.number | 6134 | - |
dc.citation.startPage | 875 | - |
dc.citation.title | SCIENCE | - |
dc.citation.volume | 340 | - |
dc.contributor.author | Lim, Chunghun | - |
dc.contributor.author | Allada, Ravi | - |
dc.date.accessioned | 2023-12-22T04:06:59Z | - |
dc.date.available | 2023-12-22T04:06:59Z | - |
dc.date.created | 2013-07-02 | - |
dc.date.issued | 2013-05 | - |
dc.description.abstract | Evidence for transcriptional feedback in circadian timekeeping is abundant, yet little is known about the mechanisms underlying translational control. We found that ATAXIN-2 (ATX2), an RNA-associated protein involved in neurodegenerative disease, is a translational activator of the rate-limiting clock component PERIOD (PER) in Drosophila. ATX2 specifically interacted with TWENTY-FOUR (TYF), an activator of PER translation. RNA interference-mediated depletion of Atx2 or the expression of a mutant ATX2 protein that does not associate with polyadenylate-binding protein (PABP) suppressed behavioral rhythms and decreased abundance of PER. Although ATX2 can repress translation, depletion of Atx2 from Drosophila S2 cells inhibited translational activation by RNA-tethered TYF and disrupted the association between TYF and PABP. Thus, ATX2 coordinates an active translation complex important for PER expression and circadian rhythms. | - |
dc.identifier.bibliographicCitation | SCIENCE, v.340, no.6134, pp.875 - 879 | - |
dc.identifier.doi | 10.1126/science.1234785 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.scopusid | 2-s2.0-84877741071 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/3277 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84877741071 | - |
dc.identifier.wosid | 000318997400047 | - |
dc.language | 영어 | - |
dc.publisher | AMER ASSOC ADVANCEMENT SCIENCE | - |
dc.title | ATAXIN-2 activates PERIOD translation to sustain circadian rhythms in Drosophila | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | CLOCK | - |
dc.subject.keywordPlus | NEURONS | - |
dc.subject.keywordPlus | REPEAT | - |
dc.subject.keywordPlus | TYPE-2 | - |
dc.subject.keywordPlus | EXPANSION | - |
dc.subject.keywordPlus | PATHOLOGY | - |
dc.subject.keywordPlus | HOMOLOG | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | CLONING | - |
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