ReviewThe Journal of cell biology2012
Cell biology of spinocerebellar ataxia.
Review in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 158 citations in OpenAlex.
- Review
- Experimental Models to Study Polyglutamine Spinocerebellar Ataxias: From Mechanisms to Therapeutic Developments.Cerebellum (London, England) · 2026Review
- Decoding ATXN2 Phosphocode: Structural Insights and Therapeutic Opportunities in Disease.The protein journal · 2025Review
- Longitudinal Study and Characterization of Gait Impairment in a Mouse Model of SCA1.Cerebellum (London, England) · 2025Article
- Early and widespread cerebellar engagement during hippocampal seizures and interictal discharges.Neurobiology of disease · 2025Article
- PGT-M for spinocerebellar ataxia type 1: development of a STR panel and a report of two clinical cases.Journal of assisted reproduction and genetics · 2024Article
- Cell-Free and In Vivo Characterization of the Inhibitory Activity ofACS chemical neuroscience · 2024Article
- Loss-of-function KAmerican journal of physiology. Cell physiology · 2023Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Suppressing gain-of-function proteins via CRISPR/Cas9 system in SCA1 cells.Scientific reports · 2022Article
- The extra-cerebellar effects of spinocerebellar ataxia type 1 (SCA1): looking beyond the cerebellum.Cellular and molecular life sciences : CMLS · 2022Review
- The Molecular Basis of Spinocerebellar Ataxia Type 7.Frontiers in neuroscience · 2022Review
- Calpain-mediated proteolysis as driver and modulator of polyglutamine toxicity.Frontiers in molecular neuroscience · 2022Review
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- Preclinical Assessment of Mesenchymal-Stem-Cell-Based Therapies in Spinocerebellar Ataxia Type 3.Biomedicines · 2021Article
- New Perspectives of Gene Therapy on Polyglutamine Spinocerebellar Ataxias: From Molecular Targets to Novel Nanovectors.Pharmaceutics · 2021Review
- SNX14 deficiency-induced defective axonal mitochondrial transport in Purkinje cells underlies cerebellar ataxia and can be reversed by valproate.National science review · 2021Article
- Utilising Induced Pluripotent Stem Cells in Neurodegenerative Disease Research: Focus on Glia.International journal of molecular sciences · 2021Review
- Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1.Genes · 2020Article
- Primary open angle glaucoma genetics: The common variants and their clinical associations (Review).Molecular medicine reports · 2020Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Ataxia is a neurological disorder characterized by loss of control of body movements. Spinocerebellar ataxia (SCA), previously known as autosomal dominant cerebellar ataxia, is a biologically robust group of close to 30 progressive neurodegenerative diseases. Six SCAs, including the more prevalent SCA1, SCA2, SCA3, and SCA6 along with SCA7 and SCA17 are caused by expansion of a CAG repeat that encodes a polyglutamine tract in the affected protein. How the mutated proteins in these polyglutamine SCAs cause disease is highly debated. Recent work suggests that the mutated protein contributes to pathogenesis within the context of its "normal" cellular function. Thus, understanding the cellular function of these proteins could aid in the development of therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.