http://purl.uniprot.org/citations/26451483 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26451483 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26451483 | http://www.w3.org/2000/01/rdf-schema#comment | "Neurodegenerative diseases have been linked to inflammation, but whether altered immunomodulation plays a causative role in neurodegeneration is not clear. We show that lack of cytokine interferon-β (IFN-β) signaling causes spontaneous neurodegeneration in the absence of neurodegenerative disease-causing mutant proteins. Mice lacking Ifnb function exhibited motor and cognitive learning impairments with accompanying α-synuclein-containing Lewy bodies in the brain, as well as a reduction in dopaminergic neurons and defective dopamine signaling in the nigrostriatal region. Lack of IFN-β signaling caused defects in neuronal autophagy prior to α-synucleinopathy, which was associated with accumulation of senescent mitochondria. Recombinant IFN-β promoted neurite growth and branching, autophagy flux, and α-synuclein degradation in neurons. In addition, lentiviral IFN-β overexpression prevented dopaminergic neuron loss in a familial Parkinson's disease model. These results indicate a protective role for IFN-β in neuronal homeostasis and validate Ifnb mutant mice as a model for sporadic Lewy body and Parkinson's disease dementia."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cell.2015.08.069"xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cell.2015.08.069"xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Rubinsztein D.C."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Rubinsztein D.C."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Goldmann T."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Goldmann T."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Loreth D."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Loreth D."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Carlsson R."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Carlsson R."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Ambjoern M."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Ambjoern M."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Ejlerskov P."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Ejlerskov P."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Friis Rundsten C."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Friis Rundsten C."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Hultberg J.G."xsd:string |
http://purl.uniprot.org/citations/26451483 | http://purl.uniprot.org/core/author | "Hultberg J.G."xsd:string |