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http://purl.uniprot.org/citations/17274962http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17274962http://www.w3.org/2000/01/rdf-schema#comment"The formation of Abeta and its subsequent deposition in senile plaques are considered to be initial events that lead to a cascade of pathological changes in AD. Mediators of Abeta-induced oxidative stress are known to cause oxidative damage to macromolecules. However, the molecular mechanisms by which Abeta-induced oxidative stress leads to neuronal cell death are not fully understood. Here we show that Abeta-induced oxidative stress activates the pro-death gene BNIP3. Abeta treatment results in mitochondrial dysfunction, accumulation of reactive oxygen species, and subsequent expression of BNIP3 in rat primary cortical neurons. Pretreatment with antioxidants abolished Abeta-induced BNIP3 expression and attenuated cell death, demonstrating the role of oxidative stress in BNIP3 induction. Abeta-induced BNIP3 expression may be mediated by hypoxia-inducible factor-1 (HIF-1) because Abeta-treatment induced accumulation and nuclear translocation of HIF-1 and knock-down of HIF-1 by RNAi inhibited BNIP3 expression. Finally, knockdown of BNIP3 reduced Abeta-induced neuronal death. Together, these results suggest a potential pathological role of BNIP3 in the etiology of AD."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.org/dc/terms/identifier"doi:10.1016/j.brainres.2006.12.086"xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Ma X."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Yang X."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Zhang Z."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Zhang S."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Kong J."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Sandhu G."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/author"Geiger J.D."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/name"Brain Res"xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/pages"221-230"xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/title"Evidence of oxidative stress-induced BNIP3 expression in amyloid beta neurotoxicity."xsd:string
http://purl.uniprot.org/citations/17274962http://purl.uniprot.org/core/volume"1138"xsd:string
http://purl.uniprot.org/citations/17274962http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17274962
http://purl.uniprot.org/citations/17274962http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17274962
http://purl.uniprot.org/uniprot/#_F7FHM5-mappedCitation-17274962http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17274962
http://purl.uniprot.org/uniprot/#_M9VYP0-mappedCitation-17274962http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17274962
http://purl.uniprot.org/uniprot/#_Q9ET45-mappedCitation-17274962http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17274962
http://purl.uniprot.org/uniprot/M9VYP0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17274962
http://purl.uniprot.org/uniprot/F7FHM5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17274962
http://purl.uniprot.org/uniprot/Q9ET45http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17274962