ReviewProgress in neurobiology2012
SCA1-phosphorylation, a regulator of Ataxin-1 function and pathogenesis.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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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.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Experimental Models to Study Polyglutamine Spinocerebellar Ataxias: From Mechanisms to Therapeutic Developments.Cerebellum (London, England) · 2026Review
- Longitudinal Study and Characterization of Gait Impairment in a Mouse Model of SCA1.Cerebellum (London, England) · 2025Article
- Article
- Dual antibody strategy for high-resolution imaging of murine Purkinje cells and their dendrites across multiple layers.STAR protocols · 2022Article
- Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Pharmacological characterization of mutant huntingtin aggregate-directed PET imaging tracer candidates.Scientific reports · 2021Article
- New Perspectives of Gene Therapy on Polyglutamine Spinocerebellar Ataxias: From Molecular Targets to Novel Nanovectors.Pharmaceutics · 2021Review
- Pathogenic mechanisms underlying spinocerebellar ataxia type 1.Cellular and molecular life sciences : CMLS · 2020Review
- VRK1 functional insufficiency due to alterations in protein stability or kinase activity of human VRK1 pathogenic variants implicated in neuromotor syndromes.Scientific reports · 2019Article
- Persistent motor dysfunction despite homeostatic rescue of cerebellar morphogenesis in the Car8 waddles mutant mouse.Neural development · 2019Article
- Roles of Post-translational Modifications in Spinocerebellar Ataxias.Frontiers in cellular neuroscience · 2018Review
- Purkinje Cell Signaling Deficits in Animal Models of Ataxia.Frontiers in synaptic neuroscience · 2018Review
- Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch.Frontiers in neuroscience · 2017Review
- Progressive impairment of cerebellar mGluR signalling and its therapeutic potential for cerebellar ataxia in spinocerebellar ataxia type 1 model mice.The Journal of physiology · 2017Article
- Consensus Paper: Cerebellar Development.Cerebellum (London, England) · 2016Review
- The autosomal dominant spinocerebellar ataxias: emerging mechanistic themes suggest pervasive Purkinje cell vulnerability.Journal of neurology, neurosurgery, and psychiatry · 2015Review
- Beyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1.Molecular neurobiology · 2014Review
- Arabidopsis MSL10 has a regulated cell death signaling activity that is separable from its mechanosensitive ion channel activity.The Plant cell · 2014Article
- Oligonucleotide-based strategies to combat polyglutamine diseases.Nucleic acids research · 2014Review
- Kaleidoscopic protein-protein interactions in the life and death of ataxin-1: new strategies against protein aggregation.Trends in neurosciences · 2014Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 1 (SCA1) is one an intriguing set of nine neurodegenerative diseases caused by the expansion of a unstable trinucleotide CAG repeat where the repeat is located within the coding of the affected gene, i.e. the polyglutamine (polyQ) diseases. A gain-of-function mechanism for toxicity in SCA1, like the other polyQ diseases, is thought to have a major role in pathogenesis. Yet, the specific nature of this gain-of-function is a matter of considerable discussion. An issue concerns whether toxicity stems from the native or normal function of the affected protein versus a novel function induced by polyQ expansion. For SCA1 considerable evidence is accumulating that pathology is mediated by a polyQ-induced exaggeration of a native function of the host protein Ataxin-1 (ATXN1) and that phosphorylation of S776 regulates its interaction with other cellular protein and thereby function. In addition, this posttranslational modification modulates toxicity of ATXN1 with an expanded polyglutamine.
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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.