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http://purl.uniprot.org/citations/26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26465922http://www.w3.org/2000/01/rdf-schema#comment"Together with Parkinson's disease (PD) and dementia with Lewy bodies, multiple system atrophy (MSA) is a member of a diverse group of neurodegenerative disorders termed α-synucleinopathies. Previously, it has been shown that α-synuclein, parkin, and synphilin-1 display disease-specific transcription patterns in frontal cortex in PD, dementia with Lewy bodies, and MSA, and thus may mediate the development of α-synucleinopathies. In this study, the differential expression of α-synuclein isoforms on transcriptional and translational levels was ascertained in MSA patients in comparison with PD cases and normal controls using isoform-specific primers and exon-specific antibodies in substantia nigra, striatum, cerebellar cortex, and nucleus dentatus. These regions are severely affected by α-synuclein pathology and neurodegeneration. Furthermore, we have also investigated transcript levels for parkin and synphilin-1 isoforms. In MSA brains, α-synuclein140 and α-synuclein 112 isoform levels were significantly increased, whereas levels of the α-synuclein 126 isoform were decreased in the substantia nigra, striatum, cerebellar cortex, and nucleus dentatus versus controls. Moreover, in MSA cases, we showed increased levels of parkin isoforms lacking the N-terminal ubiquitin-like domain and an aggregation-prone synphilin-1A isoform that causes neuronal toxicity in MSA. In PD brains, parkin transcript variant 3, 7, and 11 were significantly and specifically over-expressed in the striatum and cerebellar cortex, together with synphilin-1A and 1C. The changes of isoform expression profiles in neurodegenerative diseases suggest alterations in the regulation of transcription and/or splicing events, leading to regional/cellular events that may be important for the highly increased aggregation of α-synuclein in the brain. We report differential expression of α-synuclein, parkin, and synphilin-1 isoforms in multiple system atrophy (MSA) versus Parkinson's disease and normal control brains. We have focused on brain regions that are severely affected by α-synuclein pathology and neurodegeneration in MSA. The reported changes of isoform expression profiles suggest alterations in the regulation of transcription that may be important for aggregation of α-synuclein in the brain."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.org/dc/terms/identifier"doi:10.1111/jnc.13392"xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Hyde T.M."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Pakkenberg B."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Bahl J.M."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Winge K."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Agander T.K."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Brudek T."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Rasmussen N.B."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/author"Tanassi J."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/name"J Neurochem"xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/pages"172-185"xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/title"Altered alpha-synuclein, parkin, and synphilin isoform levels in multiple system atrophy brains."xsd:string
http://purl.uniprot.org/citations/26465922http://purl.uniprot.org/core/volume"136"xsd:string
http://purl.uniprot.org/citations/26465922http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26465922
http://purl.uniprot.org/citations/26465922http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26465922
http://purl.uniprot.org/uniprot/#_D3JZW5-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_D3K2X1-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_D3K2X2-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_A0A0S2Z446-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_A0A0S2Z447-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_A0A1W5XGD7-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922
http://purl.uniprot.org/uniprot/#_A0A1W5XGE1-mappedCitation-26465922http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26465922