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http://purl.uniprot.org/citations/18187572http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18187572http://www.w3.org/2000/01/rdf-schema#comment"Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. However, the molecular mechanisms regulating neuron death after H/I injury are poorly defined and remain controversial. Here we show that Atg7, a gene essential for autophagy induction, is a critical mediator of H/I-induced neuron death. Neonatal mice subjected to H/I injury show dramatically increased autophagosome formation and extensive hippocampal neuron death that is regulated by both caspase-3-dependent and -independent execution. Mice deficient in Atg7 show nearly complete protection from both H/I-induced caspase-3 activation and neuron death indicating that Atg7 is critically positioned upstream of multiple neuronal death executioner pathways. Adult H/I brain injury also produces a significant increase in autophagy, but unlike neonatal H/I, neuron death is almost exclusively caspase-3-independent. These data suggest that autophagy plays an essential role in triggering neuronal death execution after H/I injury and Atg7 represents an attractive therapeutic target for minimizing the neurological deficits associated with H/I brain injury."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.org/dc/terms/identifier"doi:10.2353/ajpath.2008.070876"xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Tanaka K."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Koike M."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Shibata M."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Uchiyama Y."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Nagata S."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Komatsu M."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Kominami E."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Kawahara N."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Waguri S."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Gotoh K."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Kuida K."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/author"Tadakoshi M."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/name"Am J Pathol"xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/pages"454-469"xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/title"Inhibition of autophagy prevents hippocampal pyramidal neuron death after hypoxic-ischemic injury."xsd:string
http://purl.uniprot.org/citations/18187572http://purl.uniprot.org/core/volume"172"xsd:string
http://purl.uniprot.org/citations/18187572http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18187572
http://purl.uniprot.org/citations/18187572http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18187572
http://purl.uniprot.org/uniprot/#_A0A0A0MQN4-mappedCitation-18187572http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18187572
http://purl.uniprot.org/uniprot/#_P70677-mappedCitation-18187572http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18187572
http://purl.uniprot.org/uniprot/#_A0A1B0GRX1-mappedCitation-18187572http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18187572