ArticleScientific reports2012
The importance of serine 776 in Ataxin-1 partner selection: a FRET analysis.
Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Human Mesenchymal Stem Cell-Derived Exosomes as Engineering Vehicles of Daunorubicin for Targeted c-Mpl+ AML Therapy.International journal of nanomedicine · 2025Article
- Pathogenic mechanisms underlying spinocerebellar ataxia type 1.Cellular and molecular life sciences : CMLS · 2020Review
- A single phosphorylation site of SIK3 regulates daily sleep amounts and sleep need in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Shade-induced nuclear localization of PIF7 is regulated by phosphorylation and 14-3-3 proteins ineLife · 2018Article
- Roles of Post-translational Modifications in Spinocerebellar Ataxias.Frontiers in cellular neuroscience · 2018Review
- Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch.Frontiers in neuroscience · 2017Review
- A Novel Interaction of Ecdysoneless (ECD) Protein with R2TP Complex Component RUVBL1 Is Required for the Functional Role of ECD in Cell Cycle Progression.Molecular and cellular biology · 2015Article
- Kaleidoscopic protein-protein interactions in the life and death of ataxin-1: new strategies against protein aggregation.Trends in neurosciences · 2014Review
- Mapping the self-association domains of ataxin-1: identification of novel non overlapping motifs.PeerJ · 2014Article
- Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Anomalous expansion of a polymorphic tract in Ataxin-1 causes the autosomal dominant spinocerebellar ataxia type 1. In addition to polyglutamine expansion, requirements for development of pathology are phosphorylation of serine 776 in Ataxin-1 and nuclear localization of the protein. The phosphorylation state of serine 776 is also crucial for selection of the Ataxin-1 multiple partners. Here, we have used FRET for an in cell study of the interaction of Ataxin-1 with the spliceosome-associated U2AF65 and the adaptor 14-3-3 proteins. Using wild-type Ataxin-1 and Ser776 mutants to a phosphomimetic aspartate and to alanine, we show that U2AF65 binds Ataxin-1 in a Ser776 phosphorylation independent manner whereas 14-3-3 interacts with phosphorylated wild-type Ataxin-1 but not with the mutants. These results indicate that Ser776 acts as the molecular switch that discriminates between normal and aberrant function and that phosphomimetics is not a generally valid approach whose applicability should be carefully validated.
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