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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Detalles Bibliográficos
Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458082/
https://www.ncbi.nlm.nih.gov/pubmed/28537272
http://dx.doi.org/10.1038/ncomms15462

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458082/
https://www.ncbi.nlm.nih.gov/pubmed/28537272
http://dx.doi.org/10.1038/ncomms15462

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