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http://purl.uniprot.org/citations/21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21549315http://www.w3.org/2000/01/rdf-schema#comment"Altered mitochondrial functionality can extend organism life span, but the underlying mechanisms are obscure. Here we report that inactivating SOV1, a member of the yeast mitochondrial translation control (MTC) module, causes a robust Sir2-dependent extension of replicative life span in the absence of respiration and without affecting oxidative damage. We found that SOV1 interacts genetically with the cAMP-PKA pathway and the chromatin remodeling apparatus. Consistently, Sov1p-deficient cells displayed reduced cAMP-PKA signaling and an elevated, Sir2p-dependent, genomic silencing. Both increased silencing and life span extension in sov1Δ cells require the PKA/Msn2/4p target Pnc1p, which scavenges nicotinamide, a Sir2p inhibitor. Inactivating other members of the MTC module also resulted in Sir2p-dependent life span extension. The data demonstrate that the nuclear silencing apparatus senses and responds to the absence of MTC proteins and that this response converges with a pathway for life span extension elicited by reducing TOR signaling."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2011.03.021"xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Liu B."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Hao X."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Molin M."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Nachin L."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Kvint K."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Nystrom T."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Caballero A."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Ugidos A."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Oling D."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/author"Mignat C."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/name"Mol Cell"xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/pages"390-400"xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/title"Absence of mitochondrial translation control proteins extends life span by activating sirtuin-dependent silencing."xsd:string
http://purl.uniprot.org/citations/21549315http://purl.uniprot.org/core/volume"42"xsd:string
http://purl.uniprot.org/citations/21549315http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21549315
http://purl.uniprot.org/citations/21549315http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21549315
http://purl.uniprot.org/uniprot/#_P14066-mappedCitation-21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21549315
http://purl.uniprot.org/uniprot/#_A0A8H4BXR6-mappedCitation-21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21549315
http://purl.uniprot.org/uniprot/#_A0A8H8UMN9-mappedCitation-21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21549315
http://purl.uniprot.org/uniprot/#_P39112-mappedCitation-21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21549315
http://purl.uniprot.org/uniprot/#_Q04748-mappedCitation-21549315http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21549315