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Times Co-cited
Similarity
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Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.
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CAG repeat expansion in the TATA box-binding protein gene causes autosomal dominant cerebellar ataxia.
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An untranslated CTG expansion causes a novel form of spinocerebellar ataxia (SCA8)
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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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SCA17 homozygote showing Huntington's disease-like phenotype.
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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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Dentatorubral and pallidoluysian atrophy expansion of an unstable CAG trinucleotide on chromosome 12p.
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Intergenerational instability and marked anticipation in SCA-17.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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Case of spinocerebellar ataxia type 17 (SCA17) associated with only 41 repeats of the TATA-binding protein (TBP) gene.
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Intranuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3.
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Deletion at ITPR1 underlies ataxia in mice and spinocerebellar ataxia 15 in humans.
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Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death.
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Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion.
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Trinucleotide repeat expansion in SCA17/TBP in white patients with Huntington's disease-like phenotype.
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Mutations in KCND3 cause spinocerebellar ataxia type 22.
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Heterozygous deletion of ITPR1, but not SUMF1, in spinocerebellar ataxia type 16.
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Mutations in voltage-gated potassium channel KCNC3 cause degenerative and developmental central nervous system phenotypes.
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ATAXIN-1 interacts with the repressor Capicua in its native complex to cause SCA1 neuropathology.
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Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation.
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Second cistron in CACNA1A gene encodes a transcription factor mediating cerebellar development and SCA6.
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Neuroprotective effects of granulocyte-colony stimulating factor in a novel transgenic mouse model of SCA17.
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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS.
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Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19.
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Bidirectional expression of CUG and CAG expansion transcripts and intranuclear polyglutamine inclusions in spinocerebellar ataxia type 8.
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Spectrin mutations cause spinocerebellar ataxia type 5.
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Non-ATG-initiated translation directed by microsatellite expansions.
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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.