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RNA helicase SACY-1 is required for longevity caused by various genetic perturbations in Caenorhabditis elegans
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Title
RNA helicase SACY-1 is required for longevity caused by various genetic perturbations in Caenorhabditis elegans
Issued Date
2016
Citation
Seo, Mihwa. (2016). RNA helicase SACY-1 is required for longevity caused by various genetic perturbations in Caenorhabditis elegans. Cell Cycle, 15(14), 1821–1829. doi: 10.1080/15384101.2016.1183845
Type
Article
Author Keywords
Agingdaf-2CelegansHEL-1insulinIGF-1 signalingRNA helicaseSACY-1
Keywords
AgingAmino ACID SequenceBindingCC. ElegansCaenorhabditis ElegansControlled StudyDAF-16DAF-2DDX41ELEGANSFAMILYGene MutationHeat StressHEL-1Igf-1 SignalingInsulin/IGF-1 SignalingLIFE-SPANLONGEVITYNonhumanNoteOXIDATIVE STRESSPATHWAYSRNA HelicaseRNA Helicase Suppressor of Acy 4 Sterility 1SACY-1Unclassified DrugIMMUNITYINHIBITIONInsulinInsulin/IGF-1
ISSN
1538-4101
Abstract
ABSTRACT: RNA 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.
URI
http://hdl.handle.net/20.500.11750/1649
DOI
10.1080/15384101.2016.1183845
Publisher
Taylor and Francis Ltd.
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