ArticleBMC genomics2015
The pathogenic human Torsin A in Drosophila activates the unfolded protein response and increases susceptibility to oxidative stress.
Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Dystonia Versus Redox Balance: A Preliminary Assessment of Oxidative Stress in Patients.Antioxidants (Basel, Switzerland) · 2025Article
- Striatal cell-type-specific molecular signatures reveal potential therapeutic targets in a model of dystonia.Neurobiology of disease · 2025Article
- DYT-Frontiers in neuroscience · 2023Review
- An Alkaline Protease-Digestion of Silkworm Powder Enhances Its Effects Over Healthspan, Autophagy, and Mitochondria Function in a Rotenone-InducedFrontiers in nutrition · 2022Article
- The HIV protease inhibitor, ritonavir, corrects diverse brain phenotypes across development in mouse model of DYT-TOR1A dystonia.Science translational medicine · 2021Article
- The abnormal firing of Purkinje cells in the knockin mouse model of DYT1 dystonia.Brain research bulletin · 2020Article
- The effects of crizotinib in a transgenicBiology open · 2019Article
- The endoplasmic reticulum unfolded protein response varies depending on the affected region of the tissue but independently from the source of stress.Cell stress & chaperones · 2019Article
- Regulation of synaptic architecture and synaptic vesicle pools by Nervous wreck at Drosophila Type 1b glutamatergic synapses.Experimental & molecular medicine · 2018Article
- Human TorsinA can function in the yeast cytosol as a molecular chaperone.The Biochemical journal · 2017Article
- Exploring the Conserved Role of MANF in the Unfolded Protein Response in Drosophila melanogaster.PloS one · 2016Article
- Drosophila Torsin Protein Regulates Motor Control and Stress Sensitivity and Forms a Complex with Fragile-X Mental Retardation Protein.Neural plasticity · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundDystonia1 (DYT1) dystonia is caused by a glutamic acid deletion (ΔE) mutation in the gene encoding Torsin A in humans (HTorA). To investigate the unknown molecular and cellular mechanisms underlying DYT1 dystonia, we performed an unbiased proteomic analysis.
resultsWe found that the amount of proteins and transcripts of an Endoplasmic reticulum (ER) resident chaperone Heat shock protein cognate 3 (HSC3) and a mitochondria chaperone Heat Shock Protein 22 (HSP22) were significantly increased in the HTorA(ΔE)- expressing brains compared to the normal HTorA (HTorA(WT)) expressing brains. The physiological consequences included an increased susceptibility to oxidative and ER stress compared to normal HTorA(WT) flies. The alteration of transcripts of Inositol-requiring enzyme-1 (IRE1)-dependent spliced X box binding protein 1(Xbp1), several ER chaperones, a nucleotide exchange factor, Autophagy related protein 8b (ATG8b) and components of the ER associated degradation (ERAD) pathway and increased expression of the Xbp1-enhanced Green Fluorescence Protein (eGFP) in HTorA(ΔE) brains strongly indicated the activation of the unfolded protein response (UPR). In addition, perturbed expression of the UPR sensors and inducers in the HTorA(ΔE) Drosophila brains resulted in a significantly reduced life span of the flies. Furthermore, the types and quantities of proteins present in the anti-HSC3 positive microsomes in the HTorA(ΔE) brains were different from those of the HTorA(WT) brains.
conclusionTaken together, these data show that HTorA(ΔE) in Drosophila brains may activate the UPR and increase the expression of HSP22 to compensate for the toxic effects caused by HTorA(ΔE) in the brains.
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