ArticleFrontiers in cellular neuroscience2023
Reduced C9orf72 expression exacerbates polyGR toxicity in patient iPSC-derived motor neurons and a Type I protein arginine methyltransferase inhibitor reduces that toxicity.
Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Protein arginine methyltransferases as regulators of phase separation: implications in cancer and neurodegenerative diseases.European biophysics journal : EBJ · 2026Review
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- PolyGR-containing aggregates link with pathology and clinical features of Alzheimer's disease.Acta neuropathologica · 2025Article
- Targeting GeneInternational journal of molecular sciences · 2025Review
- Review
- Review
- Atypical Neuropsychiatric Presentation of FTD-ALS Caused by a Pathogenic Repeat Expansion inJournal of geriatric psychiatry and neurology · 2024Article
- Roadmap for C9ORF72 in Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Report on the C9ORF72 FTD/ALS Summit.Neurology and therapy · 2023Article
- Functional Implications of Protein Arginine Methyltransferases (PRMTs) in Neurodegenerative Diseases.Biology · 2023Review
- A toxic gain-of-function mechanism in C9orf72 ALS impairs the autophagy-lysosome pathway in neurons.Acta neuropathologica communications · 2023Article
- Translation of dipeptide repeat proteins ineLife · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Intronic repeat expansions in the Methods: To study this, we generated a panel of C9orf72 homozygous and hemizygous knockout iPSCs to examine the contribution of C9orf72 loss-of-function toward disease pathogenesis. We differentiated these iPSCs into spinal motor neurons (sMNs). Results: We found that reduced levels of C9orf72 exacerbate polyGR15 toxicity in a dose-dependent manner. Type I PRMT inhibition was able to partially rescue polyGR15 toxicity in both wild-type and C9orf72-expanded sMNs. Discussion: This study explores the interplay of loss-of-function and gain-of-function toxicity in C9orf72 ALS. It also implicates type I PRMT inhibitors as a possible modulator of polyGR toxicity.
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