ReviewFrontiers in neuroscience2020
The Mechanisms of Nuclear Proteotoxicity in Polyglutamine Spinocerebellar Ataxias.
Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Integrated Plasma and Glial Cell Evidence Indicates a Functional Role for hsa-miR-342-5p in Spinocerebellar Ataxia Type 7 and Its Potential Use as a Biomarker.International journal of molecular sciences · 2026Article
- In Silico Analysis of miRNA-Regulated Pathways in Spinocerebellar Ataxia Type 7.Current issues in molecular biology · 2025Article
- DRED: A Comprehensive Database of Genes Related to Repeat Expansion Diseases.Genomics, proteomics & bioinformatics · 2024Article
- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
- Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.MedComm · 2024Review
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- Increased nuclear import characterizes aberrant nucleocytoplasmic transport in neurons from patients with spinocerebellar ataxia type 7.Frontiers in molecular neuroscience · 2024Article
- The stress granule protein G3BP1 alleviates spinocerebellar ataxia-associated deficits.Brain : a journal of neurology · 2023Article
- CBP-Mediated Acetylation of Importin α Mediates Calcium-Dependent Nucleocytoplasmic Transport of Selective Proteins inMolecules and cells · 2022Article
- Molecular insights into the interaction of CAG trinucleotide RNA repeats with nucleolin and its implication in polyglutamine diseases.Nucleic acids research · 2022Article
- Transcription factor EB-mediated mesenchymal stem cell therapy induces autophagy and alleviates spinocerebellar ataxia type 3 defects in neuronal cells model.Cell death & disease · 2022Article
- Quality control of cytoplasmic proteins inside the nucleus.Computational and structural biotechnology journal · 2022Review
- Polyglutamine Ataxias: Our Current Molecular Understanding and What the Future Holds for Antisense Therapies.Biomedicines · 2021Review
- Ataxin-2 Dysregulation Triggers a Compensatory Fragile X Mental Retardation Protein Decrease inMolecules and cells · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine (polyQ) spinocerebellar ataxias (SCAs) are the most prevalent subset of SCAs and share the aberrant expansion of Q-encoding CAG repeats within the coding sequences of disease-responsible genes as their common genetic cause. These polyQ SCAs (SCA1, SCA2, SCA3, SCA6, SCA7, and SCA17) are inherited neurodegenerative diseases characterized by the progressive atrophy of the cerebellum and connected regions of the nervous system, which leads to loss of fine muscle movement coordination. Upon the expansion of polyQ repeats, the mutated proteins typically accumulate disproportionately in the neuronal nucleus, where they sequester various target molecules, including transcription factors and other nuclear proteins. However, it is not yet clearly understood how CAG repeat expansion takes place or how expanded polyQ proteins accumulate in the nucleus. In this article, we review the current knowledge on the molecular and cellular bases of nuclear proteotoxicity of polyQ proteins in SCAs and present our perspectives on the remaining issues surrounding these diseases.
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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.