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식물노화·수명연구단
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RNA helicase SACY-1 is required for longevity caused by various genetic perturbationsin Caenorhabditis elegans

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dc.contributor.authorMihwa Seo-
dc.contributor.authorSangsoon Park-
dc.contributor.authorHong Gil Nam-
dc.contributor.authorSeung-Jae V. Lee-
dc.date.available2016-08-23T04:24:02Z-
dc.date.created2016-08-11-
dc.date.issued2016-07-
dc.identifier.issn1538-4101-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/2740-
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. © 2016 Taylor & Francis-
dc.description.uri1-
dc.language영어-
dc.publisherLANDES BIOSCIENCE-
dc.titleRNA helicase SACY-1 is required for longevity caused by various genetic perturbationsin Caenorhabditis elegans-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000382232100010-
dc.identifier.scopusid2-s2.0-84973174670-
dc.identifier.rimsid56198ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorHong Gil Nam-
dc.identifier.doi10.1080/15384101.2016.1183845-
dc.identifier.bibliographicCitationCELL CYCLE, v.15, no.14, pp.1821 - 1829-
dc.citation.titleCELL CYCLE-
dc.citation.volume15-
dc.citation.number14-
dc.citation.startPage1821-
dc.citation.endPage1829-
dc.date.scptcdate2018-10-01-
dc.description.wostc2-
dc.description.scptc2-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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-
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-
Appears in Collections:
Center for Plant Aging Research (식물 노화·수명 연구단) > 1. Journal Papers (저널논문)
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