Selective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington's disease mice: implications for the ubiquitin–proteasomal and autophagy systems
Published 2012 View Full Article
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Title
Selective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington's disease mice: implications for the ubiquitin–proteasomal and autophagy systems
Authors
Keywords
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Journal
HUMAN MOLECULAR GENETICS
Volume 21, Issue 24, Pages 5280-5293
Publisher
Oxford University Press (OUP)
Online
2012-09-11
DOI
10.1093/hmg/dds379
References
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Note: Only part of the references are listed.- Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease
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- Ganglioside GM1 induces phosphorylation of mutant huntingtin and restores normal motor behavior in Huntington disease mice
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- Role of autophagy in histone deacetylase inhibitor-induced apoptotic and nonapoptotic cell death
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- Serines 13 and 16 Are Critical Determinants of Full-Length Human Mutant Huntingtin Induced Disease Pathogenesis in HD Mice
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- Histone deacetylase inhibitors: possible implications for neurodegenerative disorders
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- Sex-dependent Effect of BAG1 in Ameliorating Motor Deficits of Huntington Disease Transgenic Mice
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- Pimelic Diphenylamide 106 Is a Slow, Tight-binding Inhibitor of Class I Histone Deacetylases
- (2008) C. James Chou et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Impaired ubiquitin–proteasome system activity in the synapses of Huntington's disease mice
- (2008) Jianjun Wang et al. JOURNAL OF CELL BIOLOGY
- Therapeutic application of histone deacetylase inhibitors for central nervous system disorders
- (2008) Aleksey G. Kazantsev et al. NATURE REVIEWS DRUG DISCOVERY
- The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice
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- The Ubiquitin-Proteasome Pathway in Huntington's Disease
- (2008) Siddhartha Mitra et al. TheScientificWorldJOURNAL
- Clozapine increases apolipoprotein D expression in rodent brain: towards a mechanism for neuroleptic pharmacotherapy
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