ArticlePloS one2011
Hdac6 knock-out increases tubulin acetylation but does not modify disease progression in the R6/2 mouse model of Huntington's disease.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 110 citations in OpenAlex.
- A next-generation HDAC6 inhibitor for amyotrophic lateral sclerosis and frontotemporal dementia.Brain : a journal of neurology · 2026Article
- Cable Cars to the Nucleus: TM4SF1-Enriched Microdomains Conduct Signaling in Endothelial Cells for Blood Vessel Formation.International journal of molecular sciences · 2025Article
- Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).International journal of molecular medicine · 2025Review
- Tubulin Acetylation: A Critical Regulator of Microtubule Function.Results and problems in cell differentiation · 2025Review
- HDAC6 inhibition disrupts HDAC6-P300 interaction reshaping the cancer chromatin landscape.Clinical epigenetics · 2024Article
- Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.Epigenomics · 2024Review
- Abnormal protein post-translational modifications induces aggregation and abnormal deposition of protein, mediating neurodegenerative diseases.Cell & bioscience · 2024Review
- Disruption of axonal transport in neurodegeneration.The Journal of clinical investigation · 2023Review
- Sex-biased autophagy as a potential mechanism mediating sex differences in ischemic stroke outcome.Neural regeneration research · 2023Review
- Centrosomes grow aggresomes to clear waste.Nature cell biology · 2022Article
- Histone Modifications and Their Targeting in Lymphoid Malignancies.International journal of molecular sciences · 2021Review
- Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021Review
- New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021Review
- Evaluation of 5-(Trifluoromethyl)-1,2,4-oxadiazole-Based Class IIa HDAC Inhibitors for Huntington's Disease.ACS medicinal chemistry letters · 2021Article
- Mechanisms of Oocyte Maturation and Related Epigenetic Regulation.Frontiers in cell and developmental biology · 2021Review
- Article
- How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.International journal of molecular sciences · 2020Review
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- A patent review of histone deacetylase 6 inhibitors in neurodegenerative diseases (2014-2019).Expert opinion on therapeutic patents · 2020Review
- Pharmacological Inhibition of HDAC6 Attenuates NLRP3 Inflammatory Response and Protects Dopaminergic Neurons in Experimental Models of Parkinson's Disease.Frontiers in aging neuroscience · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a progressive neurodegenerative disorder for which there is no effective disease modifying treatment. Following-on from studies in HD animal models, histone deacetylase (HDAC) inhibition has emerged as an attractive therapeutic option. In parallel, several reports have demonstrated a role for histone deacetylase 6 (HDAC6) in the modulation of the toxicity caused by the accumulation of misfolded proteins, including that of expanded polyglutamine in an N-terminal huntingtin fragment. An important role for HDAC6 in kinesin-1 dependent transport of brain-derived neurotrophic factor (BDNF) from the cortex to the striatum has also been demonstrated. To elucidate the role that HDAC6 plays in HD progression, we evaluated the effects of the genetic depletion of HDAC6 in the R6/2 mouse model of HD. Loss of HDAC6 resulted in a marked increase in tubulin acetylation throughout the brain. Despite this, there was no effect on the onset and progression of a wide range of behavioural, physiological, molecular and pathological HD-related phenotypes. We observed no change in the aggregate load or in the levels of soluble mutant exon 1 transprotein. HDAC6 genetic depletion did not affect the efficiency of BDNF transport from the cortex to the striatum. Therefore, we conclude that HDAC6 inhibition does not modify disease progression in R6/2 mice and HDAC6 should not be prioritized as a therapeutic target for HD.
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