Nature Communications (May 2017)

Fibril polymorphism affects immobilized non-amyloid flanking domains of huntingtin exon1 rather than its polyglutamine core

  • Hsiang-Kai Lin,
  • Jennifer C. Boatz,
  • Inge E. Krabbendam,
  • Ravindra Kodali,
  • Zhipeng Hou,
  • Ronald Wetzel,
  • Amalia M. Dolga,
  • Michelle A. Poirier,
  • Patrick C. A. van der Wel

DOI
https://doi.org/10.1038/ncomms15462
Journal volume & issue
Vol. 8, no. 1
pp. 1 – 12

Abstract

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Huntington's disease is caused by a polyglutamine stretch expansion in the first exon of huntingtin. Here, the authors use infrared spectroscopy and solid-state NMR and show that polymorphic huntingtin exon1 fibres differ in their flanking regions but not their core polyglutamine amyloid structures.