ArticleThe Journal of biological chemistry2017
Expanded polyalanine tracts function as nuclear export signals and promote protein mislocalization via eEF1A1 factor.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Pre- and postsynaptic upregulation of FasII synergistically underlies neuropathological and behavioral phenotypes in a Drosophila model of myotonic dystrophy.Nature communications · 2025Article
- Direct and Indirect Protein Interactions Link FUS Aggregation to Histone Post-Translational Modification Dysregulation and Growth Suppression in an ALS/FTD Yeast Model.Journal of fungi (Basel, Switzerland) · 2025Article
- Disease-associated polyalanine expansion mutations impair UBA6-dependent ubiquitination.The EMBO journal · 2024Article
- Localization and Functional Roles of Components of the Translation Apparatus in the Eukaryotic Cell Nucleus.Cells · 2021Review
- Evolution and expansion of the RUNX2 QA repeat corresponds with the emergence of vertebrate complexity.Communications biology · 2020Review
- Identification of proteins involved in transcription/translation (eEF 1A1) as an inhibitor of Bax induced apoptosis.Molecular biology reports · 2020Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Musashi-1: An Example of How Polyalanine Tracts Contribute to Self-Association in the Intrinsically Disordered Regions of RNA-Binding Proteins.International journal of molecular sciences · 2020Article
- Immunodeficiency in a Patient with 22q11.2 Distal Deletion Syndrome and a p.Ala7dup Variant in theMolecular syndromology · 2020Article
- Research Advances on Therapeutic Approaches to Congenital Central Hypoventilation Syndrome (CCHS).Frontiers in neuroscience · 2020Review
- Mitochondrial localization of PABPN1 in oculopharyngeal muscular dystrophy.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Article
- Repeat expansion diseases.Handbook of clinical neurology · 2018Review
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyalanine (poly(A)) diseases are caused by the expansion of translated GCN triplet nucleotide sequences encoding poly(A) tracts in proteins. To date, nine human disorders have been found to be associated with poly(A) tract expansions, including congenital central hypoventilation syndrome and oculopharyngeal muscular dystrophy. Previous studies have demonstrated that unexpanded wild-type poly(A)-containing proteins localize to the cell nucleus, whereas expanded poly(A)-containing proteins primarily localize to the cytoplasm. Because most of these poly(A) disease proteins are transcription factors, this mislocalization causes cellular transcriptional dysregulation leading to cellular dysfunction. Correcting this faulty localization could potentially point to strategies to treat the aforementioned disorders, so there is a pressing need to identify the mechanisms underlying the mislocalization of expanded poly(A) protein. Here, we performed a glutathione
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