Histone deacetylase 6 inhibition compensates for the transport deficit in Huntington's disease by increasing tubulin acetylation.

@article{Dompierre2007HistoneD6,
  title={Histone deacetylase 6 inhibition compensates for the transport deficit in Huntington's disease by increasing tubulin acetylation.},
  author={Jim P Dompierre and Juliette D. Godin and B{\'e}n{\'e}dicte C. Charrin and Fabrice P Cordeli{\`e}res and Stephen J. King and Sandrine Humbert and Fr{\'e}d{\'e}ric Saudou},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2007},
  volume={27 13},
  pages={3571-83}
}
A defect in microtubule (MT)-based transport contributes to the neuronal toxicity observed in Huntington's disease (HD). Histone deacetylase (HDAC) inhibitors show neuroprotective effects in this devastating neurodegenerative disorder. We report here that HDAC inhibitors, including trichostatin A (TSA), increase vesicular transport of brain-derived neurotrophic factor (BDNF) by inhibiting HDAC6, thereby increasing acetylation at lysine 40 of alpha-tubulin. MT acetylation in vitro and in cells… CONTINUE READING
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