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http://purl.uniprot.org/citations/20807312http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20807312http://www.w3.org/2000/01/rdf-schema#comment"Recent studies provided evidence that chromogranins can interact with mutant superoxide dismutase 1 (SOD1) and that chromogranin B (CgB) may act as a susceptibility gene and modifier of onset in amyotrophic lateral sclerosis (ALS). To further investigate the role of chromogranins in ALS pathogenesis, we generated SOD1(G37R) mice that over-express CgA under the control of Thy1 promoter. Here, we report that neuronal over-expression of CgA in SOD1(G37R) mice caused acceleration of onset of motor impairment and exacerbation of motor neuron degeneration. The use of monoclonal antibody specific to misfolded mutant SOD1 demonstrated a higher level of misfolded SOD1 species in double transgenic mice compared to SOD1(G37R) mice, suggesting a stabilization of pathogenic SOD1 species by excess CgA. These results suggest a role of chromogranins as modulators of disease onset in ALS pathogenesis."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.org/dc/terms/identifier"doi:10.1111/j.1471-4159.2010.06979.x"xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/author"Julien J.P."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/author"Lariviere R."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/author"Urushitani M."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/author"Ezzi S.A."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/name"J Neurochem"xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/pages"1102-1111"xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/title"Neuronal over-expression of chromogranin A accelerates disease onset in a mouse model of ALS."xsd:string
http://purl.uniprot.org/citations/20807312http://purl.uniprot.org/core/volume"115"xsd:string
http://purl.uniprot.org/citations/20807312http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20807312
http://purl.uniprot.org/citations/20807312http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20807312
http://purl.uniprot.org/uniprot/#_G5E968-mappedCitation-20807312http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20807312
http://purl.uniprot.org/uniprot/#_Q86T07-mappedCitation-20807312http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20807312
http://purl.uniprot.org/uniprot/#_P10645-mappedCitation-20807312http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20807312
http://purl.uniprot.org/uniprot/Q86T07http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20807312
http://purl.uniprot.org/uniprot/P10645http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20807312
http://purl.uniprot.org/uniprot/G5E968http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20807312