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http://purl.uniprot.org/citations/11580896http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11580896http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11580896http://www.w3.org/2000/01/rdf-schema#comment"In C. elegans, a hyperactivated MEC-4(d) ion channel induces necrotic-like neuronal death that is distinct from apoptosis. We report that null mutations in calreticulin suppress both mec-4(d)-induced cell death and the necrotic cell death induced by expression of a constitutively activated Galpha(S) subunit. RNAi-mediated knockdown of calnexin, mutations in the ER Ca(2+) release channels unc-68 (ryanodine receptor) or itr-1 (inositol 1,4,5 triphosphate receptor), and pharmacological manipulations that block ER Ca(2+) release also suppress death. Conversely, thapsigargin-induced ER Ca(2+) release can restore mec-4(d)-induced cell death when calreticulin is absent. We conclude that high [Ca(2+)](i) is a requirement for necrosis in C. elegans and suggest that an essential step in the death mechanism is release of ER-based Ca(2+) stores. ER-driven Ca(2+) release has previously been implicated in mammalian necrosis, suggesting necrotic death mechanisms may be conserved."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.org/dc/terms/identifier"doi:10.1016/s0896-6273(01)00432-9"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.org/dc/terms/identifier"doi:10.1016/s0896-6273(01)00432-9"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Xu K."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Xu K."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Tavernarakis N."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Tavernarakis N."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Driscoll M."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/author"Driscoll M."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/name"Neuron"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/name"Neuron"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/pages"957-971"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/pages"957-971"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/title"Necrotic cell death in C. elegans requires the function of calreticulin and regulators of Ca(2+) release from the endoplasmic reticulum."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/title"Necrotic cell death in C. elegans requires the function of calreticulin and regulators of Ca(2+) release from the endoplasmic reticulum."xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/11580896http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/11580896http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11580896
http://purl.uniprot.org/citations/11580896http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11580896
http://purl.uniprot.org/citations/11580896http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11580896
http://purl.uniprot.org/citations/11580896http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11580896