ReviewNeurobiology of disease2011
Molecular pathways in dystonia.
Review in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Spiking Patterns in the Globus Pallidus Highlight Convergent Neural Dynamics across Diverse Genetic Dystonia Syndromes.Annals of neurology · 2025Article
- Mutation in Prkra results in cerebellar abnormality and reduced eIF2α phosphorylation in a model of DYT-PRKRA.Disease models & mechanisms · 2024Article
- A frameshift mutation in the murinebioRxiv : the preprint server for biology · 2024Article
- Transcriptional regulatory network for neuron-glia interactions and its implication for DYT6 dystonia.Dystonia (Lausanne, Switzerland) · 2023Article
- DYT-Biomolecules · 2022Article
- A pathogenic DYT-THAP1 dystonia mutation causes hypomyelination and loss of YY1 binding.Human molecular genetics · 2022Article
- Dystonia-specific mutations in THAP1 alter transcription of genes associated with neurodevelopment and myelin.American journal of human genetics · 2021Article
- TorsinA folding and N-linked glycosylation are sensitive to redox homeostasis.Biochimica et biophysica acta. Molecular cell research · 2021Article
- Dystonia 16 (DYT16) mutations in PACT cause dysregulated PKR activation and eIF2α signaling leading to a compromised stress response.Neurobiology of disease · 2020Article
- THAP11 Functions as a Tumor Suppressor in Gastric Cancer through Regulating c-Myc Signaling Pathways.BioMed research international · 2020Article
- Article
- A truncated PACT protein resulting from a frameshift mutation reported in movement disorder DYT16 triggers caspase activation and apoptosis.Journal of cellular biochemistry · 2019Article
- Han Chinese family with early-onset Parkinson's disease carries novel compound heterozygous mutations in the PARK2 gene.Brain and behavior · 2019Article
- Mutations in THAP1/DYT6 reveal that diverse dystonia genes disrupt similar neuronal pathways and functions.PLoS genetics · 2018Article
- Early-onset torsion dystonia: a novel high-throughput yeast genetic screen for factors modifying protein levels of torsinAΔE.Disease models & mechanisms · 2017Article
- Using the shared genetics of dystonia and ataxia to unravel their pathogenesis.Neuroscience and biobehavioral reviews · 2017Review
- Deep brain stimulation for myoclonus-dystonia syndrome with double mutations in DYT1 and DYT11.Scientific reports · 2017Article
- Article
- Altered activation of protein kinase PKR and enhanced apoptosis in dystonia cells carrying a mutation in PKR activator protein PACT.The Journal of biological chemistry · 2015Article
- Mutant human torsinA, responsible for early-onset dystonia, dominantly suppresses GTPCH expression, dopamine levels and locomotion in Drosophila melanogaster.Biology open · 2015Article
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Authors and funding
5 authors.
Funding
Abstract
The hereditary dystonias comprise a set of diseases defined by a common constellation of motor deficits. These disorders are most likely associated with different molecular etiologies, many of which have yet to be elucidated. Here we discuss recent advances in three forms of hereditary dystonia, DYT1, DYT6 and DYT16, which share a similar clinical picture: onset in childhood or adolescence, progressive spread of symptoms with generalized involvement of body regions and a steady state affliction without treatment. Unlike DYT1, the genes responsible for DYT6 and DYT16 have only recently been identified, with relatively little information about the function of the encoded proteins. Nevertheless, recent data suggest that these proteins may fit together within interacting pathways involved in dopaminergic signaling, transcriptional regulation, and cellular stress responses. This review focuses on these molecular pathways, highlighting potential common themes among these dystonias which may serve as areas for future research. This article is part of a Special Issue entitled "Advances 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.