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Ataxin-1

Known as: Ataxin 1, Spinocerebellar Ataxia Type 1 Protein, SCA1 Protein 
A chromatin-binding factor that represses Notch signaling and associates with RNA. Expansion of the polyglutamine tract by expanded CAG repeats in… 
National Institutes of Health

Related topics

Related topics

10 relations
ATXN1 geneAtaxia, SpinocerebellarIn BloodProcess of secretion

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
Highly Cited
2013
Highly Cited
2013
Synthesis of TAT peptide-tagged PEGylated chitosan nanoparticles for siRNA delivery targeting neurodegenerative diseases.
Highly Cited
2013
Highly Cited
2013
An Out-of-frame Overlapping Reading Frame in the Ataxin-1 Coding Sequence Encodes a Novel Ataxin-1 Interacting Protein*
Background: The spinocerebellar ataxia type 1 (SCA1) gene encoding ataxin-1 (ATXN1) contains an alternative open reading frame… 
Highly Cited
2013
Highly Cited
2013
RAS–MAPK–MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1
Many neurodegenerative disorders, such as Alzheimer’s, Parkinson’s and polyglutamine diseases, share a common pathogenic… 
Highly Cited
2010
Highly Cited
2010
Partial Loss of Ataxin-1 Function Contributes to Transcriptional Dysregulation in Spinocerebellar Ataxia Type 1 Pathogenesis
Spinocerebellar ataxia type 1 (SCA1) is a dominantly inherited neurodegenerative disease caused by expansion of a CAG repeat that… 
Highly Cited
2007
Highly Cited
2007
dAtaxin-2 Mediates Expanded Ataxin-1-Induced Neurodegeneration in a Drosophila Model of SCA1
Spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of neurodegenerative disorders sharing atrophy of the… 
Highly Cited
2007
Highly Cited
2007
Phosphorylation of ataxin-3 by glycogen synthase kinase 3beta at serine 256 regulates the aggregation of ataxin-3.
Highly Cited
2001
Highly Cited
2001
Altered trafficking of membrane proteins in purkinje cells of SCA1 transgenic mice.
Highly Cited
1998
Highly Cited
1998
Nuclear Inclusions in Glutamine Repeat Disorders Are They Pernicious, Coincidental, or Beneficial?
Review
1998
Review
1998
Neuronal Intranuclear Inclusions in Polyglutamine Diseases Nuclear Weapons or Nuclear Fallout?
Review
1997
Review
1997
Intranuclear Neuronal Inclusions: A Common Pathogenic Mechanism for Glutamine-Repeat Neurodegenerative Diseases?
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