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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Xehetasun bibliografikoak
Argitaratua izan da:Nat Commun
Egile Nagusiak: 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.
Formatua: Artigo
Hizkuntza:Inglês
Argitaratua: Nature Publishing Group 2017
Gaiak:
Article
Sarrera elektronikoa: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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