A C-terminal ataxin-2 disordered region promotes Huntingtin protein aggregation and neurodegeneration in Drosophila models of Huntington’s disease

AbstractThe Ataxin-2 (Atx2) protein contributes to the progression of neurodegenerative phenotypes in animal models of amyotrophic lateral sclerosis (ALS), type 2 spinocerebellar ataxia (SCA-2), Parkinson’s disease, and Huntington’s disease (HD). However, because the Atx2 protein contains multiple s...

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Bibliographic Details
Main Authors: Joern Huelsmeier, Emily Walker, Baskar Bakthavachalu, Mani Ramaswami
Format: Article
Language:English
Published: Oxford University Press 2021-10-01
Series:G3: Genes, Genomes, Genetics
Online Access:https://academic.oup.com/g3journal/article-lookup/doi/10.1093/g3journal/jkab355
Description
Summary:AbstractThe Ataxin-2 (Atx2) protein contributes to the progression of neurodegenerative phenotypes in animal models of amyotrophic lateral sclerosis (ALS), type 2 spinocerebellar ataxia (SCA-2), Parkinson’s disease, and Huntington’s disease (HD). However, because the Atx2 protein contains multiple separable activities, deeper understanding requires experiments to address the exact mechanisms by which Atx2 modulates neurodegeneration (ND) progression. Recent work on two ALS models, C9ORF72 and FUS, in DrosophilaDrosophila
ISSN:2160-1836