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http://purl.uniprot.org/citations/30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30776374http://www.w3.org/2000/01/rdf-schema#comment"GCN5L1 regulates mitochondrial protein acetylation, cellular bioenergetics, reactive oxygen species (ROS) generation, and organelle positioning in a number of diverse cell types. However, the functional role of GCN5L1 in the heart is currently unknown. As many of the factors regulated by GCN5L1 play a major role in ischemia-reperfusion (I/R) injury, we sought to determine if GCN5L1 is an important nexus in the response to cardiac ischemic stress. Deletion of GCN5L1 in cardiomyocytes resulted in impaired myocardial post-ischemic function and increased infarct development in isolated work-performing hearts. GCN5L1 knockout hearts displayed hallmarks of ROS damage, and scavenging of ROS restored cardiac function and reduced infarct volume in vivo. GCN5L1 knockdown in cardiac-derived AC16 cells was associated with reduced activation of the pro-survival MAP kinase ERK1/2, which was also reversed by ROS scavenging, leading to restored cell viability. We therefore conclude that GCN5L1 activity provides an important protection against I/R induced, ROS-mediated damage in the ischemic heart."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.org/dc/terms/identifier"doi:10.1016/j.yjmcc.2019.02.009"xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Zhang M."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Scott I."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Sack M.N."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Corey C."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Shiva S."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"McTiernan C.F."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Traba J."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Thapa D."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Stoner M.W."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/author"Manning J.R."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/name"J Mol Cell Cardiol"xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/pages"69-78"xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/title"Cardiac-specific deletion of GCN5L1 restricts recovery from ischemia-reperfusion injury."xsd:string
http://purl.uniprot.org/citations/30776374http://purl.uniprot.org/core/volume"129"xsd:string
http://purl.uniprot.org/citations/30776374http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30776374
http://purl.uniprot.org/citations/30776374http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30776374
http://purl.uniprot.org/uniprot/#_A0A286YDF7-mappedCitation-30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30776374
http://purl.uniprot.org/uniprot/#_D3YVM8-mappedCitation-30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30776374
http://purl.uniprot.org/uniprot/#_P78537-mappedCitation-30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30776374
http://purl.uniprot.org/uniprot/#_D3Z4L7-mappedCitation-30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30776374
http://purl.uniprot.org/uniprot/#_O55102-mappedCitation-30776374http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30776374