ArticleASN neuro2026
Polyglutamine-Expanded Ataxin-3 Accelerates CFTR Degradation Through K63-Linked Ubiquitination to Exacerbate Microglial Inflammation.
Article in ASN neuro, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
The deubiquitinase Ataxin-3 causes spinocerebellar ataxia type 3 (SCA3) upon polyglutamine (polyQ) expansion. While expressed in the nervous system, the function of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel therein remains unclear, as does its potential regulation by Ataxin-3. This study reveals that Ataxin-3 interacts with and promotes CFTR degradation in human microglia by its K63-linked polyubiquitination, thereby shortening CFTR's half-life. Paradoxically, K63-linked polyubiquitin chains also promote the degradation of Ataxin-3 itself, suggesting a complex feedback mechanism. The pathogenic Ataxin-3Q80 mutant exerts a stronger effect than the wild-type protein. Consequently, this Ataxin-3-CFTR axis drives microglial polarization toward a pro-inflammatory phenotype and amplifies neuroinflammation. We thus identify a novel "Ataxin-3-K63 ubiquitin chain-CFTR" pathway that controls microglial activation, offering new mechanistic insight and therapeutic targets for SCA3.
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