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Times Cited: 75
Times Cited: 75
Times Cited
Times Co-cited
Similarity
Autosomal dominant cerebellar ataxias: polyglutamine expansions and beyond.
Alexandra Durr. Lancet Neurol 2010
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Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha 1A-voltage-dependent calcium channel.
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CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1.
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Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2.
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Deletion at ITPR1 underlies ataxia in mice and spinocerebellar ataxia 15 in humans.
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Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.
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Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 2.
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Cloning of the SCA7 gene reveals a highly unstable CAG repeat expansion.
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Spectrin mutations cause spinocerebellar ataxia type 5.
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RORalpha-mediated Purkinje cell development determines disease severity in adult SCA1 mice.
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Mutations in KCND3 cause spinocerebellar ataxia type 22.
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Missense mutations in ITPR1 cause autosomal dominant congenital nonprogressive spinocerebellar ataxia.
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Mutations in voltage-gated potassium channel KCNC3 cause degenerative and developmental central nervous system phenotypes.
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Nuclear localization or inclusion body formation of ataxin-2 are not necessary for SCA2 pathogenesis in mouse or human.
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Do mutations in the murine ataxia gene TRPC3 cause cerebellar ataxia in humans?
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Clinical features, neurogenetics and neuropathology of the polyglutamine spinocerebellar ataxias type 1, 2, 3, 6 and 7.
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Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19.
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Expansion of intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36, a type of spinocerebellar ataxia accompanied by motor neuron involvement.
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Scale for the assessment and rating of ataxia: development of a new clinical scale.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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The autosomal dominant spinocerebellar ataxias: emerging mechanistic themes suggest pervasive Purkinje cell vulnerability.
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Excitation-induced ataxin-3 aggregation in neurons from patients with Machado-Joseph disease.
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Antisense oligonucleotide therapy for spinocerebellar ataxia type 2.
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Missense mutations in the regulatory domain of PKC gamma: a new mechanism for dominant nonepisodic cerebellar ataxia.
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Gene profiling links SCA1 pathophysiology to glutamate signaling in Purkinje cells of transgenic mice.
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A conserved eEF2 coding variant in SCA26 leads to loss of translational fidelity and increased susceptibility to proteostatic insult.
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Expanding the clinical phenotype associated with ELOVL4 mutation: study of a large French-Canadian family with autosomal dominant spinocerebellar ataxia and erythrokeratodermia.
Maxime Cadieux-Dion, Maude Turcotte-Gauthier, Anne Noreau, Caroline Martin, Caroline Meloche, Micheline Gravel, Christian Allen Drouin, Guy A Rouleau, Dang Khoa Nguyen, Patrick Cossette. JAMA Neurol 2014
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SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein.
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Identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and cloning technique, DIRECT.
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Second cistron in CACNA1A gene encodes a transcription factor mediating cerebellar development and SCA6.
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Mutations in the mitochondrial protease gene AFG3L2 cause dominant hereditary ataxia SCA28.
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Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 3.
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Deranged calcium signaling in Purkinje cells and pathogenesis in spinocerebellar ataxia 2 (SCA2) and other ataxias.
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Changes in Purkinje cell firing and gene expression precede behavioral pathology in a mouse model of SCA2.
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Mutant β-III spectrin causes mGluR1α mislocalization and functional deficits in a mouse model of spinocerebellar ataxia type 5.
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RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia.
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Abnormalities in the climbing fiber-Purkinje cell circuitry contribute to neuronal dysfunction in ATXN1[82Q] mice.
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A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia.
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An miRNA-mediated therapy for SCA6 blocks IRES-driven translation of the CACNA1A second cistron.
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Polyglutamine spinocerebellar ataxias - from genes to potential treatments.
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Cellular and molecular pathways triggering neurodegeneration in the spinocerebellar ataxias.
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Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.
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RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1.
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TGM6 identified as a novel causative gene of spinocerebellar ataxias using exome sequencing.
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8
Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.