TorsinA: movement at many levels.

Neuron

Molecular Neurogenetics Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, 02129, Boston, MA, USA.

Published: July 2001

TorsinA is the causative protein in the human neurologic disease early onset torsin dystonia, a movement disorder involving dysfunction in the basal ganglia without apparent neurodegeneration. Most cases result from a dominantly acting three-base pair deletion in the TOR1A gene causing loss of a glutamic acid near the carboxyl terminus of torsinA. Torsins are members of the AAA(+) superfamily of ATPases and are present in all multicellular organisms. Initial studies suggest that torsinA is an ER protein involved in chaperone functions and/or membrane movement.

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http://dx.doi.org/10.1016/s0896-6273(01)00350-6DOI Listing

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