ArticleFrontiers in genetics2019
The FMRpolyGlycine Protein Mediates Aggregate Formation and Toxicity Independent of the CGG mRNA Hairpin in a Cellular Model for FXTAS.
Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Integrative transcriptome-wide association analyses reveal PRKCG-linked GABAergic dysfunction in Fragile X-associated tremor/ataxia syndrome.Nature communications · 2026Article
- IGF2BPs directly regulate the noncanonical translation of toxic proteins from mutant FMR1 mRNA containing expanded CGG repeats.Nature communications · 2025Article
- Polyglycine-mediated aggregation of FAM98B disrupts tRNA processing in GGC repeat disorders.Science (New York, N.Y.) · 2025Article
- Advances on the Mechanisms and Therapeutic Strategies in Non-coding CGG Repeat Expansion Diseases.Molecular neurobiology · 2024Review
- Microglia contribute to polyG-dependent neurodegeneration in neuronal intranuclear inclusion disease.Acta neuropathologica · 2024Article
- FXTAS Neuropathology Includes Widespread Reactive Astrogliosis and White Matter Specific Astrocyte Degeneration.Annals of neurology · 2024Article
- Native functions of short tandem repeats.eLife · 2023Article
- CGG repeats trigger translational frameshifts that generate aggregation-prone chimeric proteins.Nucleic acids research · 2022Article
- Mechanistic convergence across initiation sites for RAN translation in fragile X associated tremor ataxia syndrome.Human molecular genetics · 2022Article
- Article
- RAN proteins in neurodegenerative disease: Repeating themes and unifying therapeutic strategies.Current opinion in neurobiology · 2022Review
- Trinucleotide CGG Repeat Diseases: An Expanding Field of Polyglycine Proteins?Frontiers in genetics · 2022Review
- Non-canonical DNA/RNA structures associated with the pathogenesis of Fragile X-associated tremor/ataxia syndrome and Fragile X syndrome.Frontiers in genetics · 2022Review
- Molecular Pathogenesis and Peripheral Monitoring of Adult Fragile X-Associated Syndromes.International journal of molecular sciences · 2021Review
- Human oncoprotein 5MP suppresses general and repeat-associated non-AUG translation via eIF3 by a common mechanism.Cell reports · 2021Article
- Fragile X syndrome and associated disorders: Clinical aspects and pathology.Neurobiology of disease · 2020Review
- Cerebellar-cortical function and connectivity during sensorimotor behavior in aging FMR1 gene premutation carriers.NeuroImage. Clinical · 2020Article
- Translation from the Ribosome to the Clinic: Implication in Neurological Disorders and New Perspectives from Recent Advances.Biomolecules · 2019Review
- Neuropathology of RAN translation proteins in fragile X-associated tremor/ataxia syndrome.Acta neuropathologica communications · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative disorder caused by a CGG-repeat expansion in the 5' UTR of the FMR1 gene on the X-chromosome. Both elevated levels of the expanded FMR1 mRNA and aberrant expression of a polyglycine protein (FMRpolyG) from the CGG-repeat region are hypothesized to trigger the pathogenesis of FXTAS. While increased expression of FMRpolyG leads to higher toxicity in FXTAS models, the pathogenic effect of this protein has only been studied in the presence of CGG-containing mRNA. Here we present a model that allows measurement of the effect of FMRpolyG-expression without co-expression of the corresponding CGG mRNA hairpin. This allows direct comparison of the effect of the FMRpolyG protein
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