RNA helicase SACY-1 is required for longevity caused by various genetic perturbations in Caenorhabditis elegans

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dc.contributor.authorSeo, Mihwako
dc.contributor.authorPark, Sangsoonko
dc.contributor.authorNam, Hong Gilko
dc.contributor.authorLee, Seung-Jae V.ko
dc.date.accessioned2019-03-19T01:28:20Z-
dc.date.available2019-03-19T01:28:20Z-
dc.date.created2019-03-06-
dc.date.issued2016-
dc.identifier.citationCELL CYCLE, v.15, no.14, pp.1821 - 1829-
dc.identifier.issn1538-4101-
dc.identifier.urihttp://hdl.handle.net/10203/251686-
dc.description.abstractRNA helicases, which unwind RNAs, are essential for RNA metabolism and homeostasis. However, the roles of RNA helicases in specific physiological processes remain poorly understood. We recently reported that an RNA helicase, HEL-1, promotes long lifespan conferred by reduced insulin/insulin-like growth factor-1 (IGF-1) signaling (IIS) in Caenorhabditis elegans. We also showed that HEL-1 induces the expression of longevity genes by physically interacting with Forkhead box O (FOXO) transcription factor. Thus, the HEL-1 RNA helicase appears to regulate lifespan by specifically activating FOXO in IIS. In the current study, we report another longevity-promoting RNA helicase, Suppressor of ACY-4 sterility 1 (SACY-1). SACY-1 contributed to the longevity of daf-2/insulin/IGF-1 receptor mutants. Unlike HEL-1, SACY-1 was also required for the longevity due to mutations in genes involved in non-IIS pathways. Thus, SACY-1 appears to function as a general longevity factor for various signaling pathways, which is different from the specific function of HEL-1.-
dc.languageEnglish-
dc.publisherTAYLOR & FRANCIS INC-
dc.titleRNA helicase SACY-1 is required for longevity caused by various genetic perturbations in Caenorhabditis elegans-
dc.typeArticle-
dc.identifier.wosid000382232100010-
dc.identifier.scopusid2-s2.0-84973174670-
dc.type.rimsART-
dc.citation.volume15-
dc.citation.issue14-
dc.citation.beginningpage1821-
dc.citation.endingpage1829-
dc.citation.publicationnameCELL CYCLE-
dc.identifier.doi10.1080/15384101.2016.1183845-
dc.contributor.localauthorLee, Seung-Jae V.-
dc.contributor.nonIdAuthorSeo, Mihwa-
dc.contributor.nonIdAuthorPark, Sangsoon-
dc.contributor.nonIdAuthorNam, Hong Gil-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorAging-
dc.subject.keywordAuthordaf-2-
dc.subject.keywordAuthorC-
dc.subject.keywordAuthorelegans-
dc.subject.keywordAuthorHEL-1-
dc.subject.keywordAuthorinsulin-
dc.subject.keywordAuthorIGF-1 signaling-
dc.subject.keywordAuthorRNA helicase-
dc.subject.keywordAuthorSACY-1-
dc.subject.keywordPlusLIFE-SPAN-
dc.subject.keywordPlusC. ELEGANS-
dc.subject.keywordPlusDAF-16-
dc.subject.keywordPlusDDX41-
dc.subject.keywordPlusBINDING-
dc.subject.keywordPlusFAMILY-
dc.subject.keywordPlusINSULIN/IGF-1-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusIMMUNITY-
dc.subject.keywordPlusPATHWAYS-
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