Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
about
Lamina-associated polypeptide 1: protein interactions and tissue-selective functionsTorsinA hypofunction causes abnormal twisting movements and sensorimotor circuit neurodegenerationA novel conditional knock-in approach defines molecular and circuit effects of the DYT1 dystonia mutation.Tor1a+/- mice develop dystonia-like movements via a striatal dopaminergic dysregulation triggered by peripheral nerve injury.Dietary regimens modify early onset of obesity in mice haploinsufficient for Rai1.Rapid genotyping of animals followed by establishing primary cultures of brain neurons.Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons.Mouse models of neurodevelopmental disease of the basal ganglia and associated circuits.The ubiquitin ligase F-box/G-domain protein 1 promotes the degradation of the disease-linked protein torsinA through the ubiquitin-proteasome pathway and macroautophagy.A dystonia-like movement disorder with brain and spinal neuronal defects is caused by mutation of the mouse laminin β1 subunit, Lamb1.Engineering animal models of dystoniaNeuronal Nuclear Membrane Budding Occurs during a Developmental Window Modulated by Torsin Paralogs.A role for cerebellum in the hereditary dystonia DYT1.Current Opinions and Areas of Consensus on the Role of the Cerebellum in Dystonia.Motor phenotypes and molecular networks associated with germline deficiency of Ciz1.Postnatal loss of P/Q-type channels confined to rhombic-lip-derived neurons alters synaptic transmission at the parallel fiber to purkinje cell synapse and replicates genomic Cacna1a mutation phenotype of ataxia and seizures in mice.Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal modelsNeurogenesis and neuronal migration in the forebrain of the TorsinA knockout mouse embryo.Functional Genomic Analyses of Mendelian and Sporadic Disease Identify Impaired eIF2α Signaling as a Generalizable Mechanism for Dystonia.New twist defines a spectrum of TOR1A neurological disease.Miniature release events of glutamate from hippocampal neurons are influenced by the dystonia-associated protein torsinA.
P2860
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P2860
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
description
2012 nî lūn-bûn
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2012 թուականին հրատարակուած գիտական յօդուած
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2012 թվականին հրատարակված գիտական հոդված
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2012年の論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年论文
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name
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@ast
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@en
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@nl
type
label
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@ast
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@en
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@nl
prefLabel
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@ast
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@en
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@nl
P2860
P3181
P1433
P1476
Genetic background modulates the phenotype of a mouse model of DYT1 dystonia
@en
P2093
Caitlin Martin
P2860
P304
P3181
P356
10.1371/JOURNAL.PONE.0032245
P407
P577
2012-01-01T00:00:00Z