Pages that link to "Q34311667"

The following pages link to Characterization of Atp1a3 mutant mice as a model of rapid-onset dystonia with parkinsonism. (Q34311667):

Displaying 37 items.

• The neural substrates of rapid-onset Dystonia-Parkinsonism (Q24609728) (← links)
• Insights into the Pathology of the α3 Na( )/K( )-ATPase Ion Pump in Neurological Disorders; Lessons from Animal Models (Q26744625) (← links)
• The Influence of Na( ), K( )-ATPase on Glutamate Signaling in Neurodegenerative Diseases and Senescence (Q26745558) (← links)
• Cognitive deficits caused by a disease-mutation in the α3 Na( )/K( )-ATPase isoform (Q27315555) (← links)
• Alternating hemiplegia of childhood-related neural and behavioural phenotypes in Na ,K -ATPase α3 missense mutant mice (Q27331805) (← links)
• Methamphetamine and inflammatory cytokines increase neuronal Na /K -ATPase isoform 3: relevance for HIV associated neurocognitive disorders (Q28483960) (← links)
• Motor restlessness, sleep disturbances, thermal sensory alterations and elevated serum iron levels in Btbd9 mutant mice (Q28585548) (← links)
• Deficits in social behavioral tests in a mouse model of alternating hemiplegia of childhood. (Q30380725) (← links)
• Cholinergic dysregulation produced by selective inactivation of the dystonia-associated protein torsinA. (Q31061478) (← links)
• Motor deficits and decreased striatal dopamine receptor 2 binding activity in the striatum-specific Dyt1 conditional knockout mice (Q34023627) (← links)
• Abnormal nuclear envelope in the cerebellar Purkinje cells and impaired motor learning in DYT11 myoclonus-dystonia mouse models (Q34063055) (← links)
• Distinct neurological disorders with ATP1A3 mutations (Q34546995) (← links)
• Behavioral and electrophysiological characterization of Dyt1 heterozygous knockout mice. (Q35208664) (← links)
• Abnormal nuclear envelopes in the striatum and motor deficits in DYT11 myoclonus-dystonia mouse models (Q35688598) (← links)
• Improved motor performance in Dyt1 ΔGAG heterozygous knock-in mice by cerebellar Purkinje-cell specific Dyt1 conditional knocking-out (Q35878028) (← links)
• Alternative approaches to modeling hereditary dystonias (Q35913791) (← links)
• Aberrant Purkinje cell activity is the cause of dystonia in a shRNA-based mouse model of Rapid Onset Dystonia-Parkinsonism (Q36269315) (← links)
• Recent advances in the molecular pathogenesis of dystonia-plus syndromes and heredodegenerative dystonias. (Q36634147) (← links)
• α3Na /K -ATPase deficiency causes brain ventricle dilation and abrupt embryonic motility in zebrafish (Q36724908) (← links)
• Engineering animal models of dystonia (Q37239952) (← links)
• A role for cerebellum in the hereditary dystonia DYT1. (Q37684995) (← links)
• The expanding spectrum of neurological phenotypes in children with ATP1A3 mutations, Alternating Hemiplegia of Childhood, Rapid-onset Dystonia-Parkinsonism, CAPOS and beyond (Q38275252) (← links)
• CAOS-Episodic Cerebellar Ataxia, Areflexia, Optic Atrophy, and Sensorineural Hearing Loss: A Third Allelic Disorder of the ATP1A3 Gene (Q38431638) (← links)
• Sodium pump regulation of locomotor control circuits (Q38766484) (← links)
• Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal models (Q41890579) (← links)
• Sodium Pumps Mediate Activity-Dependent Changes in Mammalian Motor Networks. (Q42055934) (← links)
• Enhanced inhibitory neurotransmission in the cerebellar cortex of Atp1a3-deficient heterozygous mice. (Q42438187) (← links)
• Electromyographic evidence in support of a knock-in mouse model of DYT1 Dystonia (Q42755733) (← links)
• Loss of Na( )/K( )-ATPase in Drosophila photoreceptors leads to blindness and age-dependent neurodegeneration (Q42941086) (← links)
• Ionic leakage underlies a gain-of-function effect of dominant disease mutations affecting diverse P-type ATPases. (Q44898847) (← links)
• Atp1a3-deficient heterozygous mice show lower rank in the hierarchy and altered social behavior. (Q47645347) (← links)
• Knock-in mouse model of alternating hemiplegia of childhood: behavioral and electrophysiologic characterization. (Q48149416) (← links)
• Novel pregnancy-triggered episodes of CAPOS syndrome. (Q52843415) (← links)
• Loss of the dystonia gene Thap1 leads to transcriptional deficits that converge on common pathogenic pathways in dystonic syndromes (Q64786603) (← links)
• A Transgenic Mouse Model to Selectively Identify α3 Na,K-ATPase Expressing Cells in the Nervous System (Q90380709) (← links)
• Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice (Q90747980) (← links)
• Alternating Hemiplegia of Childhood: Understanding the Genotype-Phenotype Relationship of ATP1A3 Variations (Q91839992) (← links)