Polyglutamine aggregates in SCA6 Purkinje cells: A tail of two toxicities

Neurology

Volumn 56, Issue 12, 2001, Pages 1618-1619

  Gomez, Christopher M ^a  

^a UNIVERSITY OF MINNESOTA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM CHANNEL; CALCIUM CHANNEL P TYPE; CALCIUM CHANNEL Q TYPE; POLYGLUTAMINE;

ALLELE; CHANNEL GATING; EDITORIAL; HUNTINGTON CHOREA; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN FOLDING; PROTEIN PROTEIN INTERACTION; PURKINJE CELL; SPINOCEREBELLAR DEGENERATION;

EID: 0035954359     PISSN: 00283878     EISSN: None     Source Type: Journal    
DOI: 10.1212/WNL.56.12.1618     Document Type: Editorial

References (13)

1. Ion channel mutations affecting muscle and brain
2. Migraine, ataxia and epilepsy: A challenging spectrum of genetically determined calcium channelopathies
3. Glutamine repeats and neurodegeneration
4. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha1A-voltage-dependent calcium channel
5. CAG repeats in SCA6. Anticipating new clues
6. Cytoplasmic and nuclear polyglutamine aggregates in SCA6 Purkinje cells
7. Abundant expression and cytoplasmic aggregations of [alpha]1A voltage-dependent calcium channel protein associated with neuro-degeneration in spinocerebellar ataxia type 6
8. Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington's disease pathology
9. Voltage-dependent calcium channels: From structure to function
10. Spinocerebellar ataxia type 6 mutation alters P-type calcium channel function
11. The polyglutamine expansion in spinocerebellar ataxia type 6 causes a beta subunit-specific enhanced activation of P/Q-type calcium channels in Xenopus oocytes
12. Progressive ataxia due to a missense mutation in a calcium-channel gene
13. Nuclear localization or inclusion body formation of ataxin-2 are not necessary for SCA2 pathogenesis in mouse or human