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Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease.
Nat Genet. 2004 Jun;36(6):585-95. doi: 10.1038/ng1362. Epub 2004 May 16.
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Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach.
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Genome-wide RNA interference screen identifies previously undescribed regulators of polyglutamine aggregation.
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Eukaryotic proteasomes cannot digest polyglutamine sequences and release them during degradation of polyglutamine-containing proteins.
Mol Cell. 2004 Apr 9;14(1):95-104. doi: 10.1016/s1097-2765(04)00151-0.
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Huntingtin-protein interactions and the pathogenesis of Huntington's disease.
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CRE-mediated transcription is increased in Huntington's disease transgenic mice.
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The ubiquitin proteasome system in neurodegenerative diseases: sometimes the chicken, sometimes the egg.
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The hunt for huntingtin function: interaction partners tell many different stories.
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Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes.
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Huntington's disease-like phenotype due to trinucleotide repeat expansions in the TBP and JPH3 genes.
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