ArticleProceedings of the National Academy of Sciences of the United States of America2003
Oligomeric and polymeric aggregates formed by proteins containing expanded polyglutamine.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 69 citations in OpenAlex.
- Lipid composition controls the huntingtin exon 1 membrane-association and differentially modulates its flanking regions' dynamics.Protein science : a publication of the Protein Society · 2026Article
- PET imaging with [¹¹C]CHDI-00485180-R, designed as radioligand for aggregated mutant huntingtin, in people with Huntington's disease.European journal of nuclear medicine and molecular imaging · 2025Article
- Biomolecular condensates and disease pathogenesis.Science China. Life sciences · 2024Review
- Phase Transition of Huntingtin: Factors and Pathological Relevance.Frontiers in genetics · 2020Review
- Structure of Membrane-Bound Huntingtin Exon 1 Reveals Membrane Interaction and Aggregation Mechanisms.Structure (London, England : 1993) · 2019Article
- Xyloketal-derived small molecules show protective effect by decreasing mutant Huntingtin protein aggregates in Caenorhabditis elegans model of Huntington's disease.Drug design, development and therapy · 2016Article
- Polyglutamine Aggregation in Huntington Disease: Does Structure Determine Toxicity?Molecular neurobiology · 2015Review
- Integration-independent Transgenic Huntington Disease Fragment Mouse Models Reveal Distinct Phenotypes and Life Span in Vivo.The Journal of biological chemistry · 2015Article
- Detection of ubiquitinated huntingtin species in intracellular aggregates.Frontiers in molecular neuroscience · 2015Article
- Monomeric, oligomeric and polymeric proteins in huntington disease and other diseases of polyglutamine expansion.Brain sciences · 2014Article
- From pathways to targets: understanding the mechanisms behind polyglutamine disease.BioMed research international · 2014Review
- Proteomic screening for amyloid proteins.PloS one · 2014Article
- Possible role of the transglutaminases in the pathogenesis of Alzheimer's disease and other neurodegenerative diseases.International journal of Alzheimer's disease · 2011Article
- Physio-pathological roles of transglutaminase-catalyzed reactions.World journal of biological chemistry · 2010Article
- Mechanism of cis-inhibition of polyQ fibrillation by polyP: PPII oligomers and the hydrophobic effect.Biophysical journal · 2009Article
- Loss of Hsp70 exacerbates pathogenesis but not levels of fibrillar aggregates in a mouse model of Huntington's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- PolyQ-expanded ataxin-3 interacts with full-length ataxin-3 in a polyQ length-dependent manner.Neuroscience bulletin · 2008Article
- Role of tissue transglutaminase type 2 in calbindin-D28k interaction with ataxin-1.Neuroscience letters · 2007Article
- Tissue transglutaminase crosslinks ataxin-1: possible role in SCA1 pathogenesis.Neuroscience letters · 2006Article
- Novel mutations that enhance or repress the aggregation potential of SOD1.Molecular and cellular biochemistry · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neurological diseases resulting from proteins containing expanded polyglutamine (polyQ) are characteristically associated with insoluble neuronal inclusions, usually intranuclear, and neuronal death. We describe here oligomeric and polymeric aggregates formed in cells by expanded polyQ. These aggregates are not dissociated by concentrated formic acid, an extremely effective solvent for otherwise insoluble proteins. Perinuclear inclusions formed in cultured cells by expanded polyQ can be completely dissolved in concentrated formic acid, but a soluble protein oligomer containing the expanded polyQ and released by the formic acid is not dissociated to monomer. In Huntington's disease, a formic acid-resistant oligomer is present in cerebral cortex, but not in cerebellum. Cortical nuclei contain a polymeric aggregate of expanded polyQ that is insoluble in formic acid, does not enter polyacrylamide gels, but is retained on filters. This finding shows that the process of polymerization is more advanced in the cerebral cortex than in cultured cells. The resistance of oligomer and polymer to formic acid suggests the participation of covalent bonds in their stabilization.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.