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Binding of alfa-syn...
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Reyes, JuanLinköpings universitet,Avdelning för neurobiologi,Medicinska fakulteten
(författare)
Binding of alfa-synuclein oligomers to Cx32 facilitates protein uptake and transfer in neurons and oligodendrocytes
- Artikel/kapitelEngelska2019
Förlag, utgivningsår, omfång ...
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2019-04-11
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SPRINGER,2019
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electronicrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:uu-390089
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-390089URI
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https://doi.org/10.1007/s00401-019-02007-xDOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:141124515URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-158850URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
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Funding Agencies|Swedish Research Council [523-2013-2735]; Deutsche Forschungsgemeinschaft (DFG) [GRK2162]
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The intercellular transfer of alpha-synuclein (-syn) has been implicated in the progression of Parkinson's disease (PD) and multiple system atrophy (MSA). The cellular mechanisms underlying this process are now beginning to be elucidated. In this study, we demonstrate that the gap junction protein connexin-32 (Cx32) is centrally involved in the preferential uptake of -syn oligomeric assemblies (o-syn) in neurons and oligodendrocytes. In vitro, we demonstrate a clear correlation between Cx32 expression and o-syn uptake. Pharmacological and genetic strategies targeting Cx32 successfully blocked o-syn uptake. In cellular and transgenic mice modeling PD and MSA, we observed significant upregulation of Cx32 which correlates with -syn accumulation. Notably, we could alsodemonstrate a direct interaction between -syn and Cx32 in two out of four human PD cases that was absent in all four age-matched controls. These data are suggestive of a link between Cx32 and PD pathophysiology. Collectively, our results provide compelling evidence for Cx32 as a novel target for therapeutic intervention in PD and related -synucleinopathies.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Sackmann, ChristopherLinköpings universitet,Avdelning för neurobiologi,Medicinska fakulteten(Swepub:liu)chrsa69
(författare)
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Hoffmann, AlanaUniv Hosp Erlangen, Dept Mol Neurol, Erlangen, Germany
(författare)
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Svenningsson, PerKarolinska Institutet,Karolinska Inst, Sweden
(författare)
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Winkler, JürgenUniv Hosp Erlangen, Dept Mol Neurol, Erlangen, Germany
(författare)
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Ingelsson, MartinUppsala universitet,Geriatrik,Uppsala Univ, Sweden(Swepub:uu)maing121
(författare)
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Hallbeck, MartinLinköpings universitet,Avdelning för neurobiologi,Medicinska fakulteten,Region Östergötland, Klinisk patologi(Swepub:liu)marha90
(författare)
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Linköpings universitetAvdelning för neurobiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Acta Neuropathologica: SPRINGER138:1, s. 23-470001-63221432-0533
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