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Times Cited: 483
Times Cited: 483
Times Cited
Times Co-cited
Similarity
Targeted gene expression as a means of altering cell fates and generating dominant phenotypes.
A H Brand, N Perrimon. Development 1993
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Genetic suppression of polyglutamine toxicity in Drosophila.
P Kazemi-Esfarjani, S Benzer. Science 2000
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Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila.
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Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.
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RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1.
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Suppression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70.
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Expanded polyglutamine protein forms nuclear inclusions and causes neural degeneration in Drosophila.
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ATAXIN-1 interacts with the repressor Capicua in its native complex to cause SCA1 neuropathology.
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Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila.
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Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1.
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Serine 776 of ataxin-1 is critical for polyglutamine-induced disease in SCA1 transgenic mice.
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SCA1 transgenic mice: a model for neurodegeneration caused by an expanded CAG trinucleotide repeat.
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Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1.
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The AXH domain of Ataxin-1 mediates neurodegeneration through its interaction with Gfi-1/Senseless proteins.
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HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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Huntingtin interacting proteins are genetic modifiers of neurodegeneration.
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CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1.
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A conditional pan-neuronal Drosophila model of spinocerebellar ataxia 7 with a reversible adult phenotype suitable for identifying modifier genes.
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Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2.
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A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease?
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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.