Mutation of the protein kinase C site in borna disease virus phosphoprotein abrogates viral interference with neuronal signaling and restores normal synaptic activity.
about
Neurons are MHC class I-dependent targets for CD8 T cells upon neurotropic viral infectionComprehensive analysis of endogenous bornavirus-like elements in eukaryote genomesIntracerebral Borna disease virus infection of bank voles leading to peripheral spread and reverse transcription of viral RNABorna disease virus phosphoprotein impairs the developmental program controlling neurogenesis and reduces human GABAergic neurogenesis.Borna disease virus phosphoprotein modulates epigenetic signaling in neurons to control viral replicationBorna disease virus infects human neural progenitor cells and impairs neurogenesis.Borna disease virus-induced neuronal degeneration dependent on host genetic background and prevented by soluble factors.Viral interference with neuronal integrity: what can we learn from the Borna disease virus?Hippocampal expression of a virus-derived protein impairs memory in mice.Borna Disease Virus
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P2860
Mutation of the protein kinase C site in borna disease virus phosphoprotein abrogates viral interference with neuronal signaling and restores normal synaptic activity.
description
2009 nî lūn-bûn
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name
Mutation of the protein kinase ...... ores normal synaptic activity.
@en
Mutation of the protein kinase ...... ores normal synaptic activity.
@nl
type
label
Mutation of the protein kinase ...... ores normal synaptic activity.
@en
Mutation of the protein kinase ...... ores normal synaptic activity.
@nl
prefLabel
Mutation of the protein kinase ...... ores normal synaptic activity.
@en
Mutation of the protein kinase ...... ores normal synaptic activity.
@nl
P2093
P2860
P50
P1433
P1476
Mutation of the protein kinase ...... ores normal synaptic activity.
@en
P2093
Christine M A Prat
Fanny Farrugia
Gwendal Le Masson
P2860
P304
P356
10.1371/JOURNAL.PPAT.1000425
P577
2009-05-08T00:00:00Z