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

Polyglutamine expansion in the huntingtin protein is the primary genetic cause of Huntington's disease (HD). Fragments coinciding with mutant huntingtin exon1 aggregate in vivo and induce HD-like pathology in mouse models. The resulting aggregates can have different structures that affect their...

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Pubblicato in:Nat Commun
Autori principali: Lin, Hsiang-Kai, Boatz, Jennifer C., Krabbendam, Inge E., Kodali, Ravindra, Hou, Zhipeng, Wetzel, Ronald, Dolga, Amalia M., Poirier, Michelle A., van der Wel, Patrick C. A.
Natura: Artigo
Lingua:Inglês
Pubblicazione: Nature Publishing Group 2017
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Accesso online:https://ncbi.nlm.nih.gov/pmc/articles/PMC5458082/
https://ncbi.nlm.nih.gov/pubmed/28537272
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/ncomms15462
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