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Multiple pathways contribute to the pathogenesis of Huntington disease.
Li S, Li XJ
Mol Neurodegener 2006, 1:19
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Impaired ubiquitin-proteasome system activity in the synapses of Huntington's disease mice.
Wang J, Wang CE, Orr A, Tydlacka S, Li SH, Li XJ
J Cell Biol 2008 Mar 24, 180:1177-89
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Intracellular degradation of misfolded proteins in polyglutamine neurodegenerative diseases.
Li X, Li H, Li XJ
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N-terminal mutant huntingtin associates with mitochondria and impairs mitochondrial trafficking.
Orr AL, Li S, Wang CE, Li H, Wang J, Rong J, Xu X, Mastroberardino PG, Greenamyre JT, Li XJ
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Differential activities of the ubiquitin-proteasome system in neurons versus glia may account for the preferential accumulation of misfolded proteins in neurons.
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J Neurosci 2008 Dec 3, 28:13285-95
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Mitochondrial structural and functional dynamics in Huntington's disease.
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Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms.
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Huntingtin interacts with the cue domain of gp78 and inhibits gp78 binding to ubiquitin and p97/VCP.
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Comprehensive behavioral testing in the R6/2 mouse model of Huntington's disease shows no benefit from CoQ10 or minocycline.
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