Amyloid formation by mutant huntingtin: threshold, progressivity and recruitment of normal polyglutamine proteins.

@article{Huang1998AmyloidFB,
  title={Amyloid formation by mutant huntingtin: threshold, progressivity and recruitment of normal polyglutamine proteins.},
  author={Chris C Huang and Peter W Faber and Francesca Persichetti and Vivek Mittal and Jean Paul G. Vonsattel and Marcy E. MacDonald and James F. Gusella},
  journal={Somatic cell and molecular genetics},
  year={1998},
  volume={24 4},
  pages={217-33}
}
Huntington's disease (HD) is caused by an expanded CAG trinucleotide repeat encoding a tract of consecutive glutamines near the amino terminus of huntingtin, a large protein of unknown function. It has been proposed that the expanded polyglutamine stretch confers a new property on huntingtin and thereby causes cell and region-specific neurodegeneration. Genotype-phenotype correlations predict that this novel property appears above a threshold length (approximately 38 glutamines), becomes… CONTINUE READING

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