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http://purl.uniprot.org/citations/22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22057010http://www.w3.org/2000/01/rdf-schema#comment"Ubiquitous calpains (calpain I and II) are generally recognized as cytosolic proteins. Recently, mitochondrial localized calpain I (μ-calpain) has been identified. Activation of mito-μ-calpain cleaves apoptosis inducing factor (AIF), a flavoprotein located within the mitochondrial intermembrane space, in liver mitochondria, but not in brain mitochondria. We first tested if activation of mito-μ-calpain cleaves AIF in isolated heart mitochondria. A decrease in AIF content within mitochondria increases cardiac injury during ischemia-reperfusion by augmenting oxidative stress. We hypothesize that the activation of mito-μ-calpain by calcium overload during ischemia-reperfusion results in decreased AIF content within mitochondria by cleaving AIF. The μ-calpain was present within mouse heart mitochondria, mostly in the intermembrane space. Exogenous calcium treatment induced a calpain-dependent decrease of mitochondrial AIF content in isolated mouse heart mitochondria. This process was blocked by a calpain inhibitor (MDL-28170). The Mitochondrial μ-calpain activity was increased by 160 ± 15% during ischemia-reperfusion compared to time control. In contrast, the mitochondrial AIF content was decreased by 52 ± 7% during reperfusion vs. time control in the buffer perfused mouse heart. Inhibition of mito-μ-calpain using MDL-28170 decreased cardiac injury by preserving AIF content within mitochondria during ischemia-reperfusion. Thus, activation of mito-μ-calpain is required to release AIF from cardiac mitochondria. Inhibition of calpains using MDL-28170 decreases cardiac injury by inhibiting both cytosolic calpains and mito-μ-calpain during ischemia-reperfusion."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2011.10.037"xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Hu Y."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Gomez L."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Xu A."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Ross T."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Paillard M."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/author"Lesnefsky E.J."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/name"Biochem Biophys Res Commun"xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/pages"533-538"xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/title"Activation of mitochondrial mu-calpain increases AIF cleavage in cardiac mitochondria during ischemia-reperfusion."xsd:string
http://purl.uniprot.org/citations/22057010http://purl.uniprot.org/core/volume"415"xsd:string
http://purl.uniprot.org/citations/22057010http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22057010
http://purl.uniprot.org/citations/22057010http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22057010
http://purl.uniprot.org/uniprot/#_B1AU25-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_O35350-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q3TI07-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q3UDG8-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q80Y25-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q3TB79-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q3UF24-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010
http://purl.uniprot.org/uniprot/#_Q8C2J1-mappedCitation-22057010http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22057010