ArticlePloS one2012
Large-scale screen for modifiers of ataxin-3-derived polyglutamine-induced toxicity in Drosophila.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases.BMC medical genomics · 2013Pooled it
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- A Hydrophobic Cluster Modulates Long-Range Allostery in the TRMT2A RNA Recognition Motif.Journal of chemical information and modeling · 2026Article
- Glutamine missense suppressor transfer RNAs inhibit polyglutamine aggregation.Molecular therapy. Nucleic acids · 2025Article
- Spinocerebellar Ataxia Type 3 Pathophysiology-Implications for Translational Research and Clinical Studies.International journal of molecular sciences · 2024Review
- Crystal structure of the RNA-recognition motif of Drosophila melanogaster tRNA (uracil-5-)-methyltransferase homolog A.Acta crystallographica. Section F, Structural biology communications · 2024Article
- Human TRMT2A methylates tRNA and contributes to translation fidelity.Nucleic acids research · 2023Article
- Viruses in LaboratoryViruses · 2023Article
- Using Drosophila to identify naturally occurring genetic modifiers of amyloid beta 42- and tau-induced toxicity.G3 (Bethesda, Md.) · 2023Article
- The Josephin domain (JD) containing proteins are predicted to bind to the same interactors: Implications for spinocerebellar ataxia type 3 (SCA3) studies usingFrontiers in molecular neuroscience · 2023Article
- Modifier pathways in polyglutamine (PolyQ) diseases: from genetic screens to drug targets.Cellular and molecular life sciences : CMLS · 2022Review
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Small-molecule modulators of TRMT2A decrease PolyQ aggregation and PolyQ-induced cell death.Computational and structural biotechnology journal · 2022Article
- Capturing the transcription factor interactome in response to sub-lethal insecticide exposure.Current research in insect science · 2021Article
- Article
- Repeat-Associated Non-ATG Translation: Molecular Mechanisms and Contribution to Neurological Disease.Annual review of neuroscience · 2019Review
- Karyopherin α-3 is a key protein in the pathogenesis of spinocerebellar ataxia type 3 controlling the nuclear localization of ataxin-3.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- RAN translation at CGG repeats induces ubiquitin proteasome system impairment in models of fragile X-associated tremor ataxia syndrome.Human molecular genetics · 2015Article
- Quantitative interaction proteomics of neurodegenerative disease proteins.Cell reports · 2015Article
- Consensus paper: pathological mechanisms underlying neurodegeneration in spinocerebellar ataxias.Cerebellum (London, England) · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine (polyQ) diseases represent a neuropathologically heterogeneous group of disorders. The common theme of these disorders is an elongated polyQ tract in otherwise unrelated proteins. So far, only symptomatic treatment can be applied to patients suffering from polyQ diseases. Despite extensive research, the molecular mechanisms underlying polyQ-induced toxicity are largely unknown. To gain insight into polyQ pathology, we performed a large-scale RNAi screen in Drosophila to identify modifiers of toxicity induced by expression of truncated Ataxin-3 containing a disease-causing polyQ expansion. We identified various unknown modifiers of polyQ toxicity. Large-scale analysis indicated a dissociation of polyQ aggregation and toxicity.
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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.