ArticleScientific reports2016
Multiple discrete soluble aggregates influence polyglutamine toxicity in a Huntington's disease model system.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Glutamine missense suppressor transfer RNAs inhibit polyglutamine aggregation.Molecular therapy. Nucleic acids · 2025Article
- Studying C9orf72 dipeptide repeat polypeptide aggregation using an analytical ultracentrifuge equipped with fluorescence detection.Analytical biochemistry · 2025Article
- Highly Potent Peptide Therapeutics To Prevent Protein Aggregation in Huntington's Disease.ACS medicinal chemistry letters · 2023Article
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- 1-Mesityl-3-(3-Sulfonatopropyl) Imidazolium Protects Against Oxidative Stress and Delays Proteotoxicity inFrontiers in pharmacology · 2022Article
- The neuroprotective effects of fisetin, a natural flavonoid in neurodegenerative diseases: Focus on the role of oxidative stress.Frontiers in pharmacology · 2022Review
- Fluorescence-based techniques for the detection of the oligomeric status of proteins: implication in amyloidogenic diseases.European biophysics journal : EBJ · 2021Review
- Molecular Strategies to Target Protein Aggregation in Huntington's Disease.Frontiers in molecular biosciences · 2021Review
- The Discovery of Highly Potent THP Derivatives as OCTN2 Inhibitors: From Structure-Based Virtual Screening to In Vivo Biological Activity.International journal of molecular sciences · 2020Article
- Escins Isolated fromFrontiers in pharmacology · 2020Article
- Yeast Models for the Study of Amyloid-Associated Disorders and Development of Future Therapy.Frontiers in molecular biosciences · 2019Review
- Identification of a 57S translation complex containing closed-loop factors and the 60S ribosome subunit.Scientific reports · 2018Article
- Huntington's disease: the coming of age.Journal of genetics · 2018Review
- Article
- Studying Huntington's Disease in Yeast: From Mechanisms to Pharmacological Approaches.Frontiers in molecular neuroscience · 2018Review
- Sedimentation Velocity Analysis with Fluorescence Detection of Mutant Huntingtin Exon 1 Aggregation in Drosophila melanogaster and Caenorhabditis elegans.Biochemistry · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) results from expansions of polyglutamine stretches (polyQ) in the huntingtin protein (Htt) that promote protein aggregation, neurodegeneration, and death. Since the diversity and sizes of the soluble Htt-polyQ aggregates that have been linked to cytotoxicity are unknown, we investigated soluble Htt-polyQ aggregates using analytical ultracentrifugation. Soon after induction in a yeast HD model system, non-toxic Htt-25Q and cytotoxic Htt-103Q both formed soluble aggregates 29S to 200S in size. Because current models indicate that Htt-25Q does not form soluble aggregates, reevaluation of previous studies may be necessary. Only Htt-103Q aggregation behavior changed, however, with time. At 6 hr mid-sized aggregates (33S to 84S) and large aggregates (greater than 100S) became present while at 24 hr primarily only mid-sized aggregates (20S to 80S) existed. Multiple factors that decreased cytotoxicity of Htt-103Q (changing the length of or sequences adjacent to the polyQ, altering ploidy or chaperone dosage, or deleting anti-aging factors) altered the Htt-103Q aggregation pattern in which the suite of mid-sized aggregates at 6 hr were most correlative with cytotoxicity. Hence, the amelioration of HD and other neurodegenerative diseases may require increased attention to and discrimination of the dynamic alterations in soluble aggregation processes.
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