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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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| Gepubliceerd in: | Nat Commun |
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| Hoofdauteurs: | , , , , , , , , |
| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
Nature Publishing Group
2017
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| Onderwerpen: | |
| Online toegang: | 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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