+ Site Statistics
+ Search Articles
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ PDF Full Text
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Translate
+ Recently Requested

Toward understanding polyglutamine-induced neurological disease in spinocerebellar ataxia type 1

Toward understanding polyglutamine-induced neurological disease in spinocerebellar ataxia type 1

Cold Spring Harbor Symposia on Quantitative Biology 61: 649-657

(PDF emailed within 1 workday: $29.90)

Accession: 018187694

Download citation: RISBibTeXText

PMID: 9246491

Related references

Polyglutamine expansion as a common pathological epitope detected in Huntingtons disease, in Spinocerebellar ataxia 1, 2 and 3 and in autosomal dominant cerebellar ataxia type II. European Journal of Human Genetics 4(SUPPL 1): 119, 1996

The ins and outs of a polyglutamine neurodegenerative disease: spinocerebellar ataxia type 1 (SCA1). Neurobiology of Disease 7(3): 129-134, 2000

Polyglutamine disease toxicity is regulated by Nemo-like kinase in spinocerebellar ataxia type 1. Journal of Neuroscience 33(22): 9328-9336, 2013

Pathogenic mechanisms of a polyglutamine-mediated neurodegenerative disease, spinocerebellar ataxia type 1. Journal of Biological Chemistry 284(12): 7425-7429, 2008

Early changes in cerebellar physiology accompany motor dysfunction in the polyglutamine disease spinocerebellar ataxia type 3. Journal of Neuroscience 31(36): 13002-13014, 2011

Spinocerebellar ataxia type 17: latest member of polyglutamine disease group highlights unanswered questions. Archives of Neurology 61(2): 183-184, 2004

Polyglutamine aggregation in Huntington's disease and spinocerebellar ataxia type 3: similar mechanisms in aggregate formation. Neuropathology and Applied Neurobiology 42(2): 153-166, 2016

The disease protein ataxin-3 forms intranuclear aggregates in the CAG/polyglutamine disorder, spinocerebellar ataxia type 3. American Journal of Human Genetics 61(4 SUPPL ): A4, 1997

Ubiquitinated nuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3/Machado-Joseph disease. Neurology 50(4 SUPPL 4): A310, 1998

CRISPR/Cas9-Targeted Deletion of Polyglutamine in Spinocerebellar Ataxia Type 3-Derived Induced Pluripotent Stem Cells. Stem Cells and Development 27(11): 756-770, 2018

Neuropathological staging of spinocerebellar ataxia type 2 by semiquantitative 1C2-positive neuron typing. Nuclear translocation of cytoplasmic 1C2 underlies disease progression of spinocerebellar ataxia type 2. Brain Pathology 24(6): 599-606, 2015

Frequency of spinocerebellar ataxia type 1, dentatorubropallidoluysian atrophy, and Machado-Joseph disease mutations in a large group of spinocerebellar ataxia patients. Neurology 46(1): 214-218, 1996

FUS colocalizes with polyglutamine, but not with TDP-43 in neuronal intranuclear inclusions in spinocerebellar ataxia type 2. Neuropathology and Applied Neurobiology 40(3): 351-355, 2014

Intranuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3. Neuron. : 333-344, 1997

Toxicity and endocytosis of spinocerebellar ataxia type 6 polyglutamine domains: role of myosin IIb. Traffic 9(7): 1088-1100, 2008