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PMID: 11498045 Published · ppublish English Journal Article Review

TorsinA: movement at many levels.

Neuron ·Vol. 31 ·No. 1 ·2001-07-19 ·Pages 9-12

Breakefield XO, Kamm C, Hanson PI

Abstract

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.

MeSH Terms
Animals Carrier Proteins/chemistry,genetics,metabolism Dystonia Musculorum Deformans/genetics,physiopathology Humans Models, Molecular Molecular Chaperones Multigene Family Phylogeny Protein Conformation Sequence Deletion
Chemicals
Carrier Proteins Molecular Chaperones TOR1A protein, human
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Breakefield X O
Molecular Neurogenetics Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, 02129, Boston, MA, USA. breakefield@helix.mgh.harvard.edu
Kamm C
Hanson P I
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
2001-07-19
Pages
9-12
Language
English
Region
United States
NLM ID
8809320
Subset
IM
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