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Overexpression of synphilin-1 promotes clearance of soluble and misfolded alpha-synuclein without restoring the motor phenotype in aged A30P transgenic mice

dc.contributor.authorCasadei, Nicolas
dc.contributor.authorPöhler, Anne-Maria
dc.contributor.authorTomás Zapico, Cristina 
dc.contributor.authorTorres Peraza, Jesús
dc.contributor.authorSchwedhelm, Ivo
dc.contributor.authorWitz, Annemarie
dc.contributor.authorZamolo, Irina
dc.contributor.authorDe Heer, Raymond
dc.contributor.authorSpruijt, Berry
dc.contributor.authorNoldus, Lucas P. J. J.
dc.contributor.authorKlucken, Jochen
dc.contributor.authorLucas Lozano, José Javier
dc.contributor.authorKahle, Philipp J.
dc.contributor.authorKrüger, Rejko
dc.contributor.authorRiess, Olaf
dc.contributor.authorNuber, Silke
dc.date.accessioned2017-04-04T07:56:48Z
dc.date.available2017-04-04T07:56:48Z
dc.date.issued2014
dc.identifier.citationHuman Molecular Genetics, 23(3), p. 767-781 (2014); doi:10.1093/hmg/ddt467
dc.identifier.issn0964-6906
dc.identifier.issn1460-2083
dc.identifier.urihttp://hdl.handle.net/10651/41668
dc.description.sponsorshipThis work was supported by a European Commission Marie Curie Initial Training Network Grant Agreement: 215618 to O.R.; Federal Ministry of Education and Research (01GN0979), the Albert-Raps Foundation, grants of the University Hospital Erlangen (ELAN No. 08.11.05.1; IZKF No. TP9), Bavaria California Technology Center (BaCaTeC), the Bavarian State Ministry of Sciences, Research, and the Arts, ForNeuroCell, the Spanish Ministry of Science and by Fundación Ramón Areces. S.N. is a fellow of the German Parkinson Society.
dc.format.extentp. 767-781
dc.language.isoeng
dc.relation.ispartofHuman Molecular Genetics
dc.rights© The Author 2013
dc.sourceScopus
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84892468324&doi=10.1093%2fhmg%2fddt467&partnerID=40&md5=93bc219e32ea2f3a78b9e79b0ce8fc1c
dc.titleOverexpression of synphilin-1 promotes clearance of soluble and misfolded alpha-synuclein without restoring the motor phenotype in aged A30P transgenic mice
dc.typejournal article
dc.identifier.doi10.1093/hmg/ddt467
dc.relation.projectID215618
dc.relation.projectID01GN0979
dc.relation.projectIDELAN/08.11.05.1
dc.relation.projectIDIZKF/TP9
dc.relation.publisherversionhttp://dx.doi.org/10.1093/hmg/ddt467


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