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Activation of zebrafish Src family kinases by the prion protein is an amyloid-beta-sensitive signal that prevents the endocytosis and degradation of

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dc.contributor.author Sempou, Emily
dc.contributor.author Biasini, Emiliano
dc.contributor.author Pinzon-Olejua, Alejandro
dc.contributor.author Harris, David-A.
dc.contributor.author Málaga Trillo, George Edward
dc.date.accessioned 2019-02-06T14:45:59Z
dc.date.available 2019-02-06T14:45:59Z
dc.date.issued 2016
dc.identifier.uri https://hdl.handle.net/20.500.12866/5160
dc.description.abstract BACKGROUND: Prions and amyloid-beta (Abeta) oligomers trigger neurodegeneration by hijacking a poorly understood cellular signal mediated by the prion protein (PrP) at the plasma membrane. In early zebrafish embryos, PrP-1-dependent signals control cell-cell adhesion via a tyrosine phosphorylation-dependent mechanism. RESULTS: Here we report that the Src family kinases (SFKs) Fyn and Yes act downstream of PrP-1 to prevent the endocytosis and degradation of en_US
dc.language.iso eng
dc.publisher Springer
dc.relation.ispartofseries Molecular Neurodegeneration
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject Endocytosis en_US
dc.subject Amyloid beta-Peptides/metabolism en_US
dc.subject Animals en_US
dc.subject beta Catenin/metabolism en_US
dc.subject Cadherins/metabolism en_US
dc.subject Cell Adhesion/physiology en_US
dc.subject Cell Membrane/metabolism en_US
dc.subject Neurons/metabolism en_US
dc.subject Prions/metabolism en_US
dc.subject Protein Binding en_US
dc.subject Proteolysis en_US
dc.subject Signal Transduction/physiology en_US
dc.subject src-Family Kinases/metabolism en_US
dc.subject Zebrafish/metabolism en_US
dc.title Activation of zebrafish Src family kinases by the prion protein is an amyloid-beta-sensitive signal that prevents the endocytosis and degradation of en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1186/s13024-016-0076-5
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#1.06.03
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.01.04
dc.relation.issn 1750-1326


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