ArticleThe Journal of biological chemistry2009
Printor, a novel torsinA-interacting protein implicated in dystonia pathogenesis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Role of Klhl14 in senescence and epithelial-to-mesenchymal transition via TGF-β modulation.Cell death & disease · 2026Article
- KLHL14 and E-Cadherin Nuclear Co-Expression as Predicting Factor of Nonfunctioning PitNET Invasiveness: Preliminary Study.Journal of clinical medicine · 2024Article
- KLHL14 is a tumor suppressor downregulated in undifferentiated thyroid cancer.Cell death discovery · 2024Article
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- Regulation of B cell receptor-dependent NF-κB signaling by the tumor suppressor KLHL14.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Kelch-like protein 14 promotes proliferation and migration of ovarian cancer cells.International journal of clinical and experimental pathology · 2020Article
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- Hypertonia-linked protein Trak1 functions with mitofusins to promote mitochondrial tethering and fusion.Protein & cell · 2018Article
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- Parkin-mediated K63-polyubiquitination targets ubiquitin C-terminal hydrolase L1 for degradation by the autophagy-lysosome system.Cellular and molecular life sciences : CMLS · 2015Article
- TorsinA hypofunction causes abnormal twisting movements and sensorimotor circuit neurodegeneration.The Journal of clinical investigation · 2014Article
- The BiP molecular chaperone plays multiple roles during the biogenesis of torsinA, an AAA+ ATPase associated with the neurological disease early-onset torsion dystonia.The Journal of biological chemistry · 2014Article
- Current Gaps in the Understanding of the Subcellular Distribution of Exogenous and Endogenous Protein TorsinA.Tremor and other hyperkinetic movements (New York, N.Y.) · 2014Article
- Article
- Mutations associated with Charcot-Marie-Tooth disease cause SIMPLE protein mislocalization and degradation by the proteasome and aggresome-autophagy pathways.Journal of cell science · 2011Article
- CSN complex controls the stability of selected synaptic proteins via a torsinA-dependent process.The EMBO journal · 2011Article
- TorsinA and the torsinA-interacting protein printor have no impact on endoplasmic reticulum stress or protein trafficking in yeast.PloS one · 2011Article
- The early-onset torsion dystonia-associated protein, torsinA, displays molecular chaperone activity in vitro.Cell stress & chaperones · 2010Article
- A molecular mechanism underlying the neural-specific defect in torsinA mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Mutant torsinA interacts with tyrosine hydroxylase in cultured cells.Neuroscience · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Early onset generalized dystonia (DYT1) is an autosomal dominant neurological disorder caused by deletion of a single glutamate residue (torsinA DeltaE) in the C-terminal region of the AAA(+) (ATPases associated with a variety of cellular activities) protein torsinA. The pathogenic mechanism by which torsinA DeltaE mutation leads to dystonia remains unknown. Here we report the identification and characterization of a 628-amino acid novel protein, printor, that interacts with torsinA. Printor co-distributes with torsinA in multiple brain regions and co-localizes with torsinA in the endoplasmic reticulum. Interestingly, printor selectively binds to the ATP-free form but not to the ATP-bound form of torsinA, supporting a role for printor as a cofactor rather than a substrate of torsinA. The interaction of printor with torsinA is completely abolished by the dystonia-associated torsinA DeltaE mutation. Our findings suggest that printor is a new component of the DYT1 pathogenic pathway and provide a potential molecular target for therapeutic intervention in dystonia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.