ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2013
Aggregation of polyQ-extended proteins is promoted by interaction with their natural coiled-coil partners.
Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Coiled-Coil Structures Mediate the Intercellular Propagation of Huntingtin.International journal of molecular sciences · 2025Article
- Predicting the involvement of polyQ- and polyA in protein-protein interactions by their amino acid context.Heliyon · 2024Article
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- Homorepeat variability within the human population.NAR genomics and bioinformatics · 2024Article
- On the identification of potential novel therapeutic targets for spinocerebellar ataxia type 1 (SCA1) neurodegenerative disease using EvoPPI3.Journal of integrative bioinformatics · 2023Article
- ATXN2 is a target of N-terminal proteolysis.PloS one · 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
- Insights from analyses of low complexity regions with canonical methods for protein sequence comparison.Briefings in bioinformatics · 2022Article
- Analysis of Huntington's Disease Modifiers Using the Hyperbolic Mapping of the Protein Interaction Network.International journal of molecular sciences · 2022Article
- Between Interactions and Aggregates: The PolyQ Balance.Genome biology and evolution · 2021Article
- Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Low Complexity Regions in Protein Interaction Modes: An Illustration in Huntingtin.International journal of molecular sciences · 2021Article
- Dissecting the role of glutamine in seeding peptide aggregation.Computational and structural biotechnology journal · 2021Article
- Nuclear inclusions of pathogenic ataxin-1 induce oxidative stress and perturb the protein synthesis machinery.Redox biology · 2020Article
- ATXN1 N-terminal region explains the binding differences of wild-type and expanded forms.BMC medical genomics · 2019Article
- Protein Co-Aggregation Related to Amyloids: Methods of Investigation, Diversity, and Classification.International journal of molecular sciences · 2018Review
- The Information Content of Glutamine-Rich Sequences Define Protein Functional Characteristics.Proceedings of the IEEE. Institute of Electrical and Electronics Engineers · 2017Article
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- The Protein Structure Context of PolyQ Regions.PloS one · 2017Article
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4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine (polyQ) diseases are genetically inherited neurodegenerative disorders. They are caused by mutations that result in polyQ expansions of particular proteins. Mutant proteins form intranuclear aggregates, induce cytotoxicity and cause neuronal cell death. Protein interaction data suggest that polyQ regions modulate interactions between coiled-coil (CC) domains. In the case of the polyQ disease spinocerebellar ataxia type-1 (SCA1), interacting proteins with CC domains further enhance aggregation and toxicity of mutant ataxin-1 (ATXN1). Here, we suggest that CC partners interacting with the polyQ region of a mutant protein, increase its aggregation while partners that interact with a different region reduce the formation of aggregates. Computational analysis of genetic screens revealed that CC-rich proteins are highly enriched among genes that enhance pathogenicity of polyQ proteins, supporting our hypothesis. We therefore suggest that blocking interactions between mutant polyQ proteins and their CC partners might constitute a promising preventive strategy against neurodegeneration.
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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.