Neuron
Volume 67, Issue 6, 23 September 2010, Pages 929-935
ReportSCA1-like Disease in Mice Expressing Wild-Type Ataxin-1 with a Serine to Aspartic Acid Replacement at Residue 776
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Highlights
► Glutamine expansion and D776 act synergistically to shape Ataxin-1-induced disease ► D776 converts wt Ataxin-1 with 30Qs to a pathogenic protein ► Disease initiation and neural dysfunction can occur without subsequent cell death
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Present address: Program in Cellular Neuroscience, Neurodegeneration and Repair, Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA
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