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http://purl.uniprot.org/citations/23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23516302http://www.w3.org/2000/01/rdf-schema#comment"Alzheimer's disease is thought to be caused by β-amyloid peptide (Aβ)-dependent synaptic dysfunction. However, the signaling pathways connecting Aβ and synaptic dysfunction remain elusive. Here we report that Aβ transiently increases the expression level of centaurin-α1 (CentA1) in neurons, which induces a Ras-dependent association of Elk-1 with mitochondria, leading to mitochondrial and synaptic dysfunction in organotypic hippocampal slices of rats. Downregulation of the CentA1-Ras-Elk-1 pathway restored normal mitochondrial activity, spine structural plasticity, spine density, and the amplitude and frequency of miniature EPSCs in Aβ-treated neurons, whereas upregulation of the pathway was sufficient to decrease spine density. Elevations of CentA1 and association of Elk-1 with mitochondria were also observed in transgenic mice overexpressing a human mutant form of amyloid precursor protein. Therefore, the CentA1-Ras-Elk-1 signaling pathway acts on mitochondria to regulate dendritic spine density and synaptic plasticity in response to Aβ in hippocampal neurons, providing new pharmacological targets for Alzheimer's disease."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.org/dc/terms/identifier"doi:10.1523/jneurosci.2641-12.2013"xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/author"Yasuda R."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/author"Oliveira A.F."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/author"Sumner E.J."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/author"Szatmari E.M."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/name"J Neurosci"xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/pages"5367-5374"xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/title"Centaurin-alpha1-Ras-Elk-1 signaling at mitochondria mediates beta-amyloid-induced synaptic dysfunction."xsd:string
http://purl.uniprot.org/citations/23516302http://purl.uniprot.org/core/volume"33"xsd:string
http://purl.uniprot.org/citations/23516302http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23516302
http://purl.uniprot.org/citations/23516302http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23516302
http://purl.uniprot.org/uniprot/#_A6K1W8-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_A6K1W9-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_A6K1X0-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_A4GTP4-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_O88768-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_Q63629-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/#_Q9QUI9-mappedCitation-23516302http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/A6K1W8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/A6K1W9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/O88768http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23516302
http://purl.uniprot.org/uniprot/A4GTP4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23516302