Consequences of the DYT1 mutation on torsinA oligomerization and degradation
- 27 September 2008
- journal article
- Published by Elsevier in Neuroscience
- Vol. 157 (3), 588-595
- https://doi.org/10.1016/j.neuroscience.2008.09.028
Abstract
No abstract availableKeywords
This publication has 30 references indexed in Scilit:
- The Torsin-family AAA+ Protein OOC-5 Contains a Critical Disulfide Adjacent to Sensor-II That Couples Redox State to Nucleotide BindingMolecular Biology of the Cell, 2008
- Dystonia-associated mutations cause premature degradation of torsinA protein and cell-type-specific mislocalization to the nuclear envelopeHuman Molecular Genetics, 2008
- Intragenic Cis and Trans Modification of Genetic Susceptibility in DYT1 Torsion DystoniaAmerican Journal of Human Genetics, 2007
- HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPSNature, 2007
- Drug discovery in the ubiquitin–proteasome systemNature Reviews Drug Discovery, 2006
- Suppression of basal autophagy in neural cells causes neurodegenerative disease in miceNature, 2006
- Loss of autophagy in the central nervous system causes neurodegeneration in miceNature, 2006
- AAA+ proteins: have engine, will workNature Reviews Molecular Cell Biology, 2005
- Recombinant Expression, Purification, and Comparative Characterization of TorsinA and Its Torsion Dystonia-Associated Variant ΔE-TorsinABiochemistry, 2003
- The early-onset torsion dystonia gene (DYT1) encodes an ATP-binding proteinNature Genetics, 1997