ArticleHuman molecular genetics2012
Protein interacting with C kinase (PICK1) is a suppressor of spinocerebellar ataxia 3-associated neurodegeneration in Drosophila.
Article in Human molecular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Insights from cerebellar transcriptomic analysis into the pathogenesis of ataxia.JAMA neurology · 2014Trial
- Aberrant NSUN1 activity connects mLife science alliance · 2026Article
- Infantile Cerebellar-Retinal Degeneration Associated With Novel ACO2 Variants: Clinical Features and Insights From a Drosophila Model.Clinical genetics · 2025Article
- Sodium arsenite induces aggresome formation by promoting PICK1 BAR domain homodimer formation.Molecular biology of the cell · 2024Article
- Progressive degeneration in a new Drosophila model of spinocerebellar ataxia type 7.Scientific reports · 2024Article
- Progressive degeneration in a newResearch square · 2023Article
- Phenotypic defects from the expression of wild-type and pathogenic TATA-binding proteins in new Drosophila models of Spinocerebellar Ataxia Type 17.G3 (Bethesda, Md.) · 2023Article
- Toxicity of pathogenic ataxin-2 in Drosophila shows dependence on a pure CAG repeat sequence.Human molecular genetics · 2021Article
- Toxic expanded GGGGCC repeat transcription is mediated by the PAF1 complex in C9orf72-associated FTD.Nature neuroscience · 2019Article
- eIF4B and eIF4H mediate GR production from expanded G4C2 in a Drosophila model for C9orf72-associated ALS.Acta neuropathologica communications · 2019Article
- Acid-Sensing Ion Channels as Potential Therapeutic Targets in Neurodegeneration and Neuroinflammation.Mediators of inflammation · 2017Review
- Polyglutamine length-dependent toxicity from α1ACT in Drosophila models of spinocerebellar ataxia type 6.Biology open · 2016Article
- Mitochondria and Caspases Tune Nmnat-Mediated Stabilization to Promote Axon Regeneration.PLoS genetics · 2016Article
- Ubiquitination regulates the neuroprotective function of the deubiquitinase ataxin-3 in vivo.The Journal of biological chemistry · 2013Article
- Trinucleotide repeats: a structural perspective.Frontiers in neurology · 2013Article
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2 authors at 2 institutions in 1 country.
Funding
Abstract
Spinocerebellar ataxia 3 (SCA3) is the most common autosomal dominant ataxia. The disease is caused by an expansion of a CAG-trinucelotide repeat region within the coding sequence of the ATXN3 gene, and this results in an expanded polyglutamine (polyQ) tract within the Ataxin-3 protein. The polyQ expansion leads to neuronal dysfunction and cell death. Here, we tested the ability of a number of proteins that interact with Ataxin-3 to modulate SCA3 pathogenicity using Drosophila. Of 10 candidates, we found four novel enhancers and one suppressor. The suppressor, PICK1 (Protein interacting with C kinase 1), is a transport protein that regulates the trafficking of ion channel subunits involved in calcium homeostasis to and from the plasma membrane. In line with calcium homeostasis being a potential pathway mis-regulated in SCA3, we also found that down-regulation of Nach, an acid sensing ion channel, mitigates SCA3 pathogenesis in flies. Modulation of PICK1 could be targeted in other neurodegenerative diseases, as the toxicity of SCA1 and tau was also suppressed when PICK1 was down-regulated. These findings indicate that interaction proteins may define a rich source of modifier pathways to target in disease situations.
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