Synaptic dysfunction in prion diseases: a trafficking problem?
about
Transgenic fatal familial insomnia mice indicate prion infectivity-independent mechanisms of pathogenesis and phenotypic expression of disease.The elusive role of the prion protein and the mechanism of toxicity in prion disease.Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice.PrPC Undergoes Basal to Apical Transcytosis in Polarized Epithelial MDCK CellsMisfolding leads the way to unraveling signaling pathways in the pathophysiology of prion diseases.Transgenic mice recapitulate the phenotypic heterogeneity of genetic prion diseases without developing prion infectivity: Role of intracellular PrP retention in neurotoxicityPrion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.
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P2860
Synaptic dysfunction in prion diseases: a trafficking problem?
description
2013 nî lūn-bûn
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2013年の論文
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2013年学术文章
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2013年学术文章
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2013年学术文章
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2013年学术文章
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2013年学术文章
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2013年學術文章
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name
Synaptic dysfunction in prion diseases: a trafficking problem?
@en
Synaptic dysfunction in prion diseases: a trafficking problem?
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type
label
Synaptic dysfunction in prion diseases: a trafficking problem?
@en
Synaptic dysfunction in prion diseases: a trafficking problem?
@nl
prefLabel
Synaptic dysfunction in prion diseases: a trafficking problem?
@en
Synaptic dysfunction in prion diseases: a trafficking problem?
@nl
P2860
P356
P1476
Synaptic dysfunction in prion diseases: a trafficking problem?
@en
P2093
Assunta Senatore
P2860
P304
P356
10.1155/2013/543803
P577
2013-11-28T00:00:00Z