ArticleSpringerPlus2014
Intracellular complexes of the early-onset torsion dystonia-associated AAA+ ATPase TorsinA.
Article in SpringerPlus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Transgenic Mice for the Translational Study of Neuropathic Pain and Dystonia.International journal of molecular sciences · 2022Review
- TorsinA folding and N-linked glycosylation are sensitive to redox homeostasis.Biochimica et biophysica acta. Molecular cell research · 2021Article
- Resolving the TorsinA Oligomerization Conundrum: The Glycan Hypothesis.Frontiers in molecular biosciences · 2020Article
- Chaperoning Endoplasmic Reticulum-Associated Degradation (ERAD) and Protein Conformational Diseases.Cold Spring Harbor perspectives in biology · 2019Review
- Early-onset torsion dystonia: a novel high-throughput yeast genetic screen for factors modifying protein levels of torsinAΔE.Disease models & mechanisms · 2017Article
- Torsin ATPases: structural insights and functional perspectives.Current opinion in cell biology · 2016Review
- Torsins: not your typical AAA+ ATPases.Critical reviews in biochemistry and molecular biology · 2015Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
A single GAG codon deletion in the gene encoding torsinA is linked to most cases of early-onset torsion dystonia. TorsinA is an ER-localized membrane-associated ATPase from the AAA+ superfamily with an unknown biological function. We investigated the formation of oligomeric complexes of torsinA in cultured mammalian cells and found that wild type torsinA associates into a complex with a molecular weight consistent with that of a homohexamer. Interestingly, the dystonia-linked variant torsinAΔE displayed a reduced propensity to form the oligomers compared to the wild type protein. We also discovered that the deletion of the N-terminal membrane-associating region of torsinA abolished oligomer formation. Our results demonstrate that the dystonia-linked mutation in the torsinA gene produces a protein variant that is deficient in maintaining its oligomeric state and suggest that ER membrane association is required to stabilize the torsinA complex.
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Registered trials
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