Abstract
Recent evidence indicates that inhibition of histone acetyltransferases may be a primary cause of cellular pathogenesis in polyglutamine diseases such as Huntington disease; the results raise the possibility that pharmacologic manipulation of protein acetylation levels could be of therapeutic benefit.
MeSH terms
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Acetyltransferases / metabolism*
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CREB-Binding Protein
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Enzyme Inhibitors / therapeutic use
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Genetic Therapy
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Histone Deacetylase Inhibitors
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Histone Deacetylases / metabolism
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Humans
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Huntington Disease / enzymology*
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Huntington Disease / genetics*
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Huntington Disease / metabolism
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Huntington Disease / therapy
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Neurodegenerative Diseases / enzymology*
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Neurodegenerative Diseases / genetics*
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Neurodegenerative Diseases / metabolism
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Neurodegenerative Diseases / therapy
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Nuclear Proteins / metabolism
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Peptides / genetics
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Peptides / metabolism*
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Trans-Activators / metabolism
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Transcription, Genetic / genetics
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Trinucleotide Repeat Expansion / genetics
Substances
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Enzyme Inhibitors
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Histone Deacetylase Inhibitors
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Nuclear Proteins
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Peptides
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Trans-Activators
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polyglutamine
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Acetyltransferases
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CREB-Binding Protein
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CREBBP protein, human
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Histone Deacetylases