RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/18662332http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18662332http://www.w3.org/2000/01/rdf-schema#comment"Selective vulnerability of neurons is a critical feature of neurodegenerative diseases, but the underlying molecular mechanisms remain largely unknown. We here report that Omi/HtrA2, a mitochondrial protein regulating survival and apoptosis of cells, decreases selectively in striatal neurons that are most vulnerable to the Huntington's disease (HD) pathology. In microarray analysis, Omi/HtrA2 was decreased under the expression of mutant huntingtin (htt) in striatal neurons but not in cortical or cerebellar neurons. Mutant ataxin-1 (Atx-1) did not affect Omi/HtrA2 in any type of neuron. Western blot analysis of primary neurons expressing mutant htt also confirmed the selective reduction of the Omi/HtrA2 protein. Immunohistochemistry with a mutant htt-transgenic mouse line and human HD brains confirmed reduction of Omi/HtrA2 in striatal neurons. Overexpression of Omi/HtrA2 by adenovirus vector reverted mutant htt-induced cell death in primary neurons. These results collectively suggest that the homeostatic but not proapoptotic function of Omi/HtrA2 is linked to selective vulnerability of striatal neurons in HD pathology."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.org/dc/terms/identifier"doi:10.1111/j.1460-9568.2008.06323.x"xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Ito H."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Shimizu S."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Tamura T."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Arai N."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Tagawa K."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Kanazawa I."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Okazawa H."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Wanker E.E."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Enokido Y."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Qi M.L."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Oyanagi K."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/author"Inagaki R."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/name"Eur J Neurosci"xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/pages"30-40"xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/title"Omi / HtrA2 is relevant to the selective vulnerability of striatal neurons in Huntington's disease."xsd:string
http://purl.uniprot.org/citations/18662332http://purl.uniprot.org/core/volume"28"xsd:string
http://purl.uniprot.org/citations/18662332http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18662332
http://purl.uniprot.org/citations/18662332http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18662332
http://purl.uniprot.org/uniprot/A0A8I6AYW8#attribution-613280A9E7802F9AEAFA35205104DE23http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18662332
http://purl.uniprot.org/uniprot/B0BNB9#attribution-613280A9E7802F9AEAFA35205104DE23http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18662332
http://purl.uniprot.org/uniprot/A0A8I6AI60#attribution-613280A9E7802F9AEAFA35205104DE23http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18662332