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http://purl.uniprot.org/citations/30566870http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30566870http://www.w3.org/2000/01/rdf-schema#comment"Calcium is a key regulator of mitochondrial function under both normal and pathological conditions. The mechanisms linking metabolic activity to mitochondrial Ca2+ signaling remain elusive, however. Here, by monitoring mitochondrial Ca2+ transients while manipulating mitochondrial membrane potential (ΔΨm), we found that mild fluctuations in ΔΨm, which do not affect Ca2+ influx, are sufficient to strongly regulate NCLX, the major efflux pathway of Ca2+ from the mitochondria. Phosphorylation of NCLX or expression of phosphomimicking mutant (S258D) rescued NCLX activity from ΔΨm-driven allosteric inhibition. By screening ΔΨm sensitivity of NCLX mutants, we also identified amino acid residues that, through functional interaction with Ser258, control NCLX regulation. Finally, we find that glucose-driven ΔΨm changes in pancreatic β-cells control mitochondrial Ca2+ signaling primarily via NCLX regulation. Our results identify a feedback control between metabolic activity and mitochondrial Ca2+ signaling and the "safety valve" NCLX phosphorylation that can rescue Ca2+ efflux in depolarized mitochondria."xsd:string
http://purl.uniprot.org/citations/30566870http://purl.org/dc/terms/identifier"doi:10.1016/j.celrep.2018.11.084"xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/author"Sekler I."xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/author"Kostic M."xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/author"Katoshevski T."xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/name"Cell Rep"xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/pages"3465-3475.e4"xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/title"Allosteric Regulation of NCLX by Mitochondrial Membrane Potential Links the Metabolic State and Ca2+ Signaling in Mitochondria."xsd:string
http://purl.uniprot.org/citations/30566870http://purl.uniprot.org/core/volume"25"xsd:string
http://purl.uniprot.org/citations/30566870http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30566870
http://purl.uniprot.org/citations/30566870http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30566870
http://purl.uniprot.org/uniprot/#_B3KSP6-mappedCitation-30566870http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30566870
http://purl.uniprot.org/uniprot/#_B4DDJ4-mappedCitation-30566870http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30566870
http://purl.uniprot.org/uniprot/#_Q6J4K2-mappedCitation-30566870http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30566870
http://purl.uniprot.org/uniprot/Q6J4K2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30566870
http://purl.uniprot.org/uniprot/B4DDJ4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30566870
http://purl.uniprot.org/uniprot/B3KSP6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30566870