A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons.

@article{Braunstein2010APM,
  title={A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons.},
  author={Kerstin E. Braunstein and Judith Eschbach and Krisztina R{\'o}na-V{\"o}r{\"o}s and Rana Soylu and Elli Mikrouli and Yves Larmet and Fr{\'e}d{\'e}rique Ren{\'e} and Jos{\'e}-Luis Gonzalez de Aguilar and J. -P. Loeffler and H P M{\"u}ller and Selina Bucher and Thomas Kaulisch and Heiko G. Niessen and Julia Tillmanns and Kristina Fischer and Birgit Schwalenst{\"o}cker and Jan Kassubek and Bernd Pichler and Detlef Stiller and {\AA} Peters{\'e}n and Albert Christian Ludolph and Luc Dupuis},
  journal={Human molecular genetics},
  year={2010},
  volume={19 22},
  pages={4385-98}
}
The molecular motor dynein and its associated regulatory subunit dynactin have been implicated in several neurodegenerative conditions of the basal ganglia, such as Huntington's disease (HD) and Perry syndrome, an atypical Parkinson-like disease. This pathogenic role has been largely postulated from the existence of mutations in the dynactin subunit p150(Glued). However, dynactin is also able to act independently of dynein, and there is currently no direct evidence linking dynein to basal… CONTINUE READING
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