Neurobehavioral abnormalities in the dysbindin-1 mutant, sandy, on a C57BL/6J genetic background.
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The schizophrenia susceptibility factor dysbindin and its associated complex sort cargoes from cell bodies to the synapseNucleocytoplasmic shuttling of dysbindin-1, a schizophrenia-related protein, regulates synapsin I expressionThe dysbindin-containing complex (BLOC-1) in brain: developmental regulation, interaction with SNARE proteins and role in neurite outgrowthSchizophrenia susceptibility gene dysbindin regulates glutamatergic and dopaminergic functions via distinctive mechanisms in DrosophilaThe molecular basis of cognitive deficits in pervasive developmental disordersBehavioral abnormalities observed in Zfhx2-deficient mice.Gene × Environment Interactions in Schizophrenia: Evidence from Genetic Mouse ModelsDysbindin promotes the post-endocytic sorting of G protein-coupled receptors to lysosomesRole of dysbindin in dopamine receptor trafficking and cortical GABA functionNeurodevelopmental animal models of schizophrenia: role in novel drug discovery and developmentBehavioral characterization of mice overexpressing human dysbindin-1.Animal models of schizophrenia.Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways.Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia.Dysbindin-containing complexes and their proposed functions in brain: from zero to (too) many in a decade.Contribution of nonprimate animal models in understanding the etiology of schizophrenia.Modeling the positive symptoms of schizophrenia in genetically modified mice: pharmacology and methodology aspectsDysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.Mutations in the BLOC-1 subunits dysbindin and muted generate divergent and dosage-dependent phenotypes.Genetic modifiers of abnormal organelle biogenesis in a Drosophila model of BLOC-1 deficiency.Reduced rate of neural differentiation in the dentate gyrus of adult dysbindin null (sandy) mouseSynaptic dysbindin-1 reductions in schizophrenia occur in an isoform-specific manner indicating their subsynaptic location.A polymorphism in the dysbindin gene (DTNBP1) associated with multiple psychiatric disorders including schizophrenia.Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia.Dysbindin and Schizophrenia: it's dopamine and glutamate all over again.CHRONIC NEONATAL DIAZOXIDE THERAPY IS NOT ASSOCIATED WITH ADVERSE EFFECTSThe Schizophrenia-Related Protein Dysbindin-1A Is Degraded and Facilitates NF-Kappa B Activity in the NucleusQuantitative proteomic and genetic analyses of the schizophrenia susceptibility factor dysbindin identify novel roles of the biogenesis of lysosome-related organelles complex 1.Loss of dysbindin-1 in mice impairs reward-based operant learning by increasing impulsive and compulsive behaviorEpistatic interaction between COMT and DTNBP1 modulates prefrontal function in mice and in humansEffects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus.Increased dysbindin-1B isoform expression in schizophrenia and its propensity in aggresome formation.The Proteome of BLOC-1 Genetic Defects Identifies the Arp2/3 Actin Polymerization Complex to Function Downstream of the Schizophrenia Susceptibility Factor Dysbindin at the SynapseThe schizophrenia susceptibility gene DTNBP1 modulates AMPAR synaptic transmission and plasticity in the hippocampus of juvenile DBA/2J mice.Evodiamine improves congnitive abilities in SAMP8 and APP(swe)/PS1(ΔE9) transgenic mouse models of Alzheimer's disease.Dysregulation of Specialized Delay/Interference-Dependent Working Memory Following Loss of Dysbindin-1A in Schizophrenia-Related Phenotypes.Loss of dysbindin-1, a risk gene for schizophrenia, leads to impaired group 1 metabotropic glutamate receptor function in mice.Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice.Src kinase as a mediator of convergent molecular abnormalities leading to NMDAR hypoactivity in schizophrenia.Schizophrenia: the "BLOC" may be in the endosomes.
P2860
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P2860
Neurobehavioral abnormalities in the dysbindin-1 mutant, sandy, on a C57BL/6J genetic background.
description
2009 nî lūn-bûn
@nan
2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@ast
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@en
type
label
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@ast
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@en
prefLabel
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@ast
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@en
P2093
P2860
P1476
Neurobehavioral abnormalities ...... a C57BL/6J genetic background.
@en
P2093
A M Tucker
D C Richer
S E Arnold
P2860
P304
P356
10.1111/J.1601-183X.2009.00477.X
P407
P577
2009-02-11T00:00:00Z