A New Chemoenzymatic Semisynthetic Approach Provides Insight into the Role of Phosphorylation beyond Exon1 of Huntingtin and Reveals N-Terminal Fragment Length-Dependent Distinct Mechanisms of Aggregation
Author:
Affiliation:
1. Laboratory of Molecular and Chemical Biology of Neurodegeneration, School of Life Sciences, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland
Funder
CHDI Foundation
??cole Polytechnique F??d??rale de Lausanne
Publisher
American Chemical Society (ACS)
Subject
Colloid and Surface Chemistry,Biochemistry,General Chemistry,Catalysis
Link
https://pubs.acs.org/doi/pdf/10.1021/jacs.1c03108
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1. Huntington's Disease
2. Huntington's disease: from molecular pathogenesis to clinical treatment
3. Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice
4. Huntingtin forms toxic NH2-terminal fragment complexes that are promoted by the age-dependent decrease in proteasome activity
5. Small Changes, Big Impact
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