Uncontrolled SFK-mediated protein trafficking in prion and Alzheimer's disease


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MÁLAGA TRILLO, Edward, Katharina OCHS, 2016. Uncontrolled SFK-mediated protein trafficking in prion and Alzheimer's disease. In: Prion. 10(5), pp. 352-361. ISSN 1933-6896. eISSN 1933-690X

@article{Malaga Trillo2016-09-20Uncon-37513, title={Uncontrolled SFK-mediated protein trafficking in prion and Alzheimer's disease}, year={2016}, doi={10.1080/19336896.2016.1221873}, number={5}, volume={10}, issn={1933-6896}, journal={Prion}, pages={352--361}, author={Málaga Trillo, Edward and Ochs, Katharina} }

<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/37513"> <dc:contributor>Ochs, Katharina</dc:contributor> <dcterms:issued>2016-09-20</dcterms:issued> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-02-16T10:52:50Z</dcterms:available> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-02-16T10:52:50Z</dc:date> <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/37513"/> <dc:creator>Ochs, Katharina</dc:creator> <dc:contributor>Málaga Trillo, Edward</dc:contributor> <dc:creator>Málaga Trillo, Edward</dc:creator> <dcterms:abstract xml:lang="eng">Prions and Amyloid beta (Aβ) peptides induce synaptic damage via complex mechanisms that include the pathological alteration of intracellular signaling cascades. The host-encoded cellular prion protein (PrP(C)) acts as a high-affinity cell surface receptor for both toxic species and it can modulate the endocytic trafficking of the N-methyl D-aspartate (NMDA) receptor and E-cadherin adhesive complexes via Src family kinases (SFKs). Interestingly, SFK-mediated control of endocytosis is a widespread mechanism used to regulate the activity of important transmembrane proteins, including neuroreceptors for major excitatory and inhibitory neurotransmitters. Here we discuss our recent work in zebrafish and accumulating evidence suggesting that subversion of this pleiotropic regulatory mechanism by Aβ oligomers and prions explains diverse neurotransmission deficits observed in human patients and mouse models of prion and Alzheimer's neurodegeneration. While Aβ, PrP(C) and SFKs constitute potential therapeutic targets on their own, drug discovery efforts might benefit significantly from aiming at protein-protein interactions that modulate the endocytosis of specific SFK targets.</dcterms:abstract> <dc:language>eng</dc:language> <dcterms:title>Uncontrolled SFK-mediated protein trafficking in prion and Alzheimer's disease</dcterms:title> </rdf:Description> </rdf:RDF>

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