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Times Cited: 83
Times Cited: 83
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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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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Mutations in KCND3 cause spinocerebellar ataxia type 22.
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Cloning of the SCA7 gene reveals a highly unstable CAG repeat expansion.
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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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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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Gene profiling links SCA1 pathophysiology to glutamate signaling in Purkinje cells of transgenic mice.
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Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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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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SCA1 transgenic mice: a model for neurodegeneration caused by an expanded CAG trinucleotide repeat.
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A novel missense mutation in CCDC88C activates the JNK pathway and causes a dominant form of spinocerebellar ataxia.
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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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A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia.
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Antisense oligonucleotide therapy for spinocerebellar ataxia type 2.
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Polyglutamine spinocerebellar ataxias - from genes to potential treatments.
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Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.
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TGM6 identified as a novel causative gene of spinocerebellar ataxias using exome sequencing.
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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.
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SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein.
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A mutation in the fibroblast growth factor 14 gene is associated with autosomal dominant cerebellar ataxia [corrected].
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Expansion of a novel CAG trinucleotide repeat in the 5' region of PPP2R2B is associated with SCA12.
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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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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.