ArticleScientific reports2015
Conformational switch of polyglutamine-expanded huntingtin into benign aggregates leads to neuroprotective effect.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Passive immunization against phosphorylated tau improves features of Huntington's disease pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Article
- Cryo-electron tomography provides topological insights into mutant huntingtin exon 1 and polyQ aggregates.Communications biology · 2021Article
- Inhibition of p38 Mitogen-Activated Protein Kinase Ameliorates HAP40 Depletion-Induced Toxicity and Proteasomal Defect in Huntington's Disease Model.Molecular neurobiology · 2021Article
- Protofilament Structure and Supramolecular Polymorphism of Aggregated Mutant Huntingtin Exon 1.Journal of molecular biology · 2020Article
- Nanoscopic Insights of Amphiphilic Peptide against the Oligomer Assembly Process to Treat Huntington's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Discovery of a potent small molecule inhibiting Huntington's disease (HD) pathogenesis via targeting CAG repeats RNA and Poly Q protein.Scientific reports · 2019Article
- Modulation of Amyloid States by Molecular Chaperones.Cold Spring Harbor perspectives in biology · 2019Review
- Possible Role of the Polyglutamine Elongation in Evolution of Amyloid-Related Evolvability.Journal of Huntington's disease · 2018Article
- Fibril polymorphism affects immobilized non-amyloid flanking domains of huntingtin exon1 rather than its polyglutamine core.Nature communications · 2017Article
- Effects of the enlargement of polyglutamine segments on the structure and folding of ataxin-2 and ataxin-3 proteins.Journal of biomolecular structure & dynamics · 2017Article
- Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
The abundant accumulation of inclusion bodies containing polyglutamine-expanded mutant huntingtin (mHTT) aggregates is considered as the key pathological event in Huntington's disease (HD). Here, we demonstrate that FKBP12, an isomerase that exhibits reduced expression in HD, decreases the amyloidogenicity of mHTT, interrupts its oligomerization process, and structurally promotes the formation of amorphous deposits. By combining fluorescence-activated cell sorting with multiple biophysical techniques, we confirm that FKBP12 reduces the amyloid property of these ultrastructural-distinct mHTT aggregates within cells. Moreover, the neuroprotective effect of FKBP12 is demonstrated in both cellular and nematode models. Finally, we show that FKBP12 also inhibit the fibrillization process of other disease-related and aggregation-prone peptides. Our results suggest a novel function of FKBP12 in ameliorating the proteotoxicity in mHTT, which may shed light on unraveling the roles of FKBP12 in different neurodegenerative diseases and developing possible therapeutic strategies.
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