ReviewTrends in cell biology2013
PolyQ disease: misfiring of a developmental cell death program?
Review in Trends in cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 59 citations in OpenAlex.
- Disrupted Transcriptional Networks in Mammalian Cells Stably Over-Expressing Pathogenic Atrophin-1.Journal of neuroscience research · 2025Article
- Disrupted Transcriptional Networks by Mutant Atrophin-1 in a Cell Culture Model of Dentatorubral-Pallidoluysian Atrophy.bioRxiv : the preprint server for biology · 2025Article
- Insights into dentatorubral-pallidoluysian atrophy from a new Drosophila model of disease.Neurobiology of disease · 2025Article
- Structural Mapping of Protein Aggregates in Live Cells Modeling Huntington's Disease.Angewandte Chemie (International ed. in English) · 2024Article
- TDP-1 and FUST-1 co-inhibit exon inclusion and control fertility together with transcriptional regulation.Nucleic acids research · 2023Article
- TDP-1 and FUST-1 co-inhibit exon inclusion and control fertility together with transcriptional regulation.bioRxiv : the preprint server for biology · 2023Article
- The features of polyglutamine regions depend on their evolutionary stability.BMC evolutionary biology · 2020Article
- The importance of definitions in the study of polyQ regions: A tale of thresholds, impurities and sequence context.Computational and structural biotechnology journal · 2020Article
- Treadmill training increases the motor activity and neuron survival of the cerebellum in a mouse model of spinocerebellar ataxia type 1.The Kaohsiung journal of medical sciences · 2019Article
- Compound Dynamics and Combinatorial Patterns of Amino Acid Repeats Encode a System of Evolutionary and Developmental Markers.Genome biology and evolution · 2019Article
- HSP90 recognizes the N-terminus of huntingtin involved in regulation of huntingtin aggregation by USP19.Scientific reports · 2017Article
- Modulation of Molecular Chaperones in Huntington's Disease and Other Polyglutamine Disorders.Molecular neurobiology · 2017Review
- Long terminal repeats power evolution of genes and gene expression programs in mammalian oocytes and zygotes.Genome research · 2017Article
- Non-apoptotic cell death in animal development.Cell death and differentiation · 2017Review
- Cross-β Polymerization of Low Complexity Sequence Domains.Cold Spring Harbor perspectives in biology · 2017Review
- Real-time imaging of Huntingtin aggregates diverting target search and gene transcription.eLife · 2016Article
- Article
- Dramatic increase in SHP2 binding activity of Helicobacter pylori Western CagA by EPIYA-C duplication: its implications in gastric carcinogenesis.Scientific reports · 2015Article
- Glutamine and Asparagine Side Chain Hyperconjugation-Induced Structurally Sensitive Vibrations.The journal of physical chemistry. B · 2015Article
- Aggregation of Polyglutamine-expanded Ataxin 7 Protein Specifically Sequesters Ubiquitin-specific Protease 22 and Deteriorates Its Deubiquitinating Function in the Spt-Ada-Gcn5-Acetyltransferase (SAGA) Complex.The Journal of biological chemistry · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Polyglutamine (polyQ) repeat diseases are neurodegenerative ailments elicited by glutamine-encoding CAG nucleotide expansions within endogenous human genes. Despite efforts to understand the basis of these diseases, the precise mechanism of cell death remains stubbornly unclear. Much of the data seem to be consistent with a model in which toxicity is an inherent property of the polyQ repeat, whereas host protein sequences surrounding the polyQ expansion modulate severity, age of onset, and cell specificity. Recently, a gene, pqn-41, encoding a glutamine-rich protein, was found to promote normally occurring non-apoptotic cell death in Caenorhabditis elegans. Here we review evidence for toxic and modulatory roles for polyQ repeats and their host proteins, respectively, and suggest similarities with pqn-41 function. We explore the hypothesis that toxicity mediated by glutamine-rich motifs may be important not only in pathology, but also in normal development.
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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.