Expansion explosion: new clues to the pathogenesis of repeat expansion neurodegenerative diseases

This publication has 25 references indexed in Scilit:

• SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein
  Human Molecular Genetics, 2001
• Polyglutamine aggregates alter protein folding homeostasis in Caenorhabditis elegans
  Proceedings of the National Academy of Sciences, 2000
• Expanding Our Understanding of Polyglutamine Diseases through Mouse Models
  Neuron, 1999
• Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington’s disease pathology
  Proceedings of the National Academy of Sciences, 1999
• Biological Implications of the DNA Structures Associated with Disease-Causing Triplet Repeats
  American Journal of Human Genetics, 1999
• Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions
  Cell, 1998
• Expanded Polyglutamine Protein Forms Nuclear Inclusions and Causes Neural Degeneration in Drosophila
  Cell, 1998
• The human gene mutation database
  Trends in Genetics, 1997
• Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the α1A-voltage-dependent calcium channel
  Nature Genetics, 1997
• When more is less: Pathogenesis of glutamine repeat neurodegenerative diseases
  Neuron, 1995