Histone Deacetylase Inhibitors as a Therapeutic Modality in Multiple Sclerosis

Gray, Steven G.

doi:10.1002/9780470743553.ch23

Cited by 2 publications

(2 citation statements)

References 188 publications

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“…Levels of the micro-RNA miR-9/miR-9A have also been shown to be downregulated in HD [29]. In the same study this micro-RNA was shown to regulate the expression of RE1 silencing transcription factor/neuronrestrictive silencer factor (REST/NRSF), a critical repressor complex known to associate with both Htt [30], KMTs and HDACs [31]. Indeed, REST/NRSF has been shown to regulate a number of miRNAs [32,33].…”

Section: Re1 Silencing Transcription Factor/neuron-restrictive Silencer Factor (Rest/nrsf)mentioning

confidence: 99%

Targeting Histone Deacetylases for the Treatment of Huntington's Disease

Gray

2010

CNS Neuroscience & Therapeutics

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Huntington's disease is a debilitating neurodegenerative condition with significant burdens on both patient and healthcare costs. Despite the identification of the causative element, an expanded toxic polyglutamine tract in the mutant Huntingtin protein, treatment options for patients with this disease remain limited. In the following review I assess the current evidence suggesting that a family of important regulatory proteins known as histone deacetylases may be an important therapeutic target in the treatment of this disease.

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Section: Re1 Silencing Transcription Factor/neuron-restrictive Silencer Factor (Rest/nrsf)mentioning

confidence: 99%

Targeting Histone Deacetylases for the Treatment of Huntington's Disease

Gray

2010

CNS Neuroscience & Therapeutics

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“…This microRNA has been identified as a critical regulator of REST/NRSF (Packer et al 2008 ), and loss of this miRNA results in increased levels of nuclear REST/NRSF activity (Bithell et al 2009 ). As REST/NRSF has been shown to associate with Htt (Zuccato et al 2003 ), KMTs and HDACs (Gray 2009 ), this may result in aberrant regulation of gene expression. Indeed, in this context, REST/NRSF has been shown to regulate several miRNAs (Conaco et al 2006 ; Wu and Xie 2006 ).…”

Section: Consequences Of Mutant Htt and Aberrant Ptms In Hdmentioning

confidence: 99%

Targeting Huntington’s disease through histone deacetylases

Gray

2011

Clin Epigenet

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Huntington’s disease (HD) is a debilitating neurodegenerative condition with significant burdens on both patient and healthcare costs. Despite extensive research, treatment options for patients with this condition remain limited. Aberrant post-translational modification (PTM) of proteins is emerging as an important element in the pathogenesis of HD. These PTMs include acetylation, phosphorylation, methylation, sumoylation and ubiquitination. Several families of proteins are involved with the regulation of these PTMs. In this review, I discuss the current evidence linking aberrant PTMs and/or aberrant regulation of the cellular machinery regulating these PTMs to HD pathogenesis. Finally, I discuss the evidence suggesting that pharmacologically targeting one of these protein families the histone deacetylases may be of potential therapeutic benefit in the treatment of HD.

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Histone Deacetylase Inhibitors as a Therapeutic Modality in Multiple Sclerosis

Cited by 2 publications

References 188 publications

Targeting Histone Deacetylases for the Treatment of Huntington's Disease

Targeting Histone Deacetylases for the Treatment of Huntington's Disease

Targeting Huntington’s disease through histone deacetylases

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