ArticleCell cycle (Georgetown, Tex.)2015
PRMT5- mediated symmetric arginine dimethylation is attenuated by mutant huntingtin and is impaired in Huntington's disease (HD).
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Brain-derived neurotrophic factor (BDNF) epigenomic modifications and brain-related phenotypes in humans: A systematic review.Neuroscience and biobehavioral reviews · 2023Pooled it
- Clinicopathological and Prognostic Significance of PRMT5 in Cancers: A System Review and Meta-Analysis.Cancer control : journal of the Moffitt Cancer CenterPooled it
- PRMT5-Cacna1d axis maintains calcium homeostasis to regulate postnatal motor development in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Diagnostic and Prognostic Value of Epigenetic Markers in Neurological Diseases. A Narrative Review.Cellular and molecular neurobiology · 2026Review
- PRMT5 Aggravates Parkinson's Disease Progression Through the Inhibition of Neuronal Autophagy Through DKK1.Neurochemical research · 2025Article
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- Review
- Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.Cellular and molecular neurobiology · 2025Review
- Alternative Splicing Analysis Reveals Adrenergic Signaling as a Novel Target for Protein Arginine Methyltransferase 5 (PRMT5) in the Heart.International journal of molecular sciences · 2025Article
- Opposing roles of p38α-mediated phosphorylation and PRMT1-mediated arginine methylation in driving TDP-43 proteinopathy.Cell reports · 2025Article
- SART3 reads methylarginine-marked glycine- and arginine-rich motifs.Cell reports · 2024Article
- Neuroinflammation and the role of epigenetic-based therapies for Huntington's disease management: the new paradigm.Inflammopharmacology · 2024Review
- Protein arginine methyltransferase 4 modulates nitric oxide synthase uncoupling and cerebral blood flow in Alzheimer's disease.Journal of cellular physiology · 2024Article
- Article
- Review
- Arginine methylation of RNA-binding proteins is impaired in Huntington's disease.Human molecular genetics · 2023Article
- Critical Roles of Protein Arginine Methylation in the Central Nervous System.Molecular neurobiology · 2023Review
- Functional Implications of Protein Arginine Methyltransferases (PRMTs) in Neurodegenerative Diseases.Biology · 2023Review
- Review
- Interaction of huntingtin with PRMTs and its subsequent arginine methylation affects HTT solubility, phase transition behavior and neuronal toxicity.Human molecular genetics · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal protein interactions of mutant huntingtin (Htt) triggered by polyglutamine expansion are thought to mediate Huntington's disease (HD) pathogenesis. Here, we explored a functional interaction of Htt with protein arginine methyltransferase 5 (PRMT5), an enzyme mediating symmetrical dimethylation of arginine (sDMA) of key cellular proteins, including histones, and spliceosomal Sm proteins. Gene transcription and RNA splicing are impaired in HD. We demonstrated PRMT5 and Htt interaction and their co-localization in transfected neurons and in HD brain. As a result of this interaction, normal (but to a lesser extend mutant) Htt stimulated PRMT5 activity in vitro. SDMA of histones H2A and H4 was reduced in the presence of mutant Htt in primary cultured neurons and in HD brain, consistent with a demonstrated reduction in R3Me2s occupancy at the transcriptionally repressed promoters in HD brain. SDMA of another PRMT5 substrate, Cajal body marker coilin, was also reduced in the HD mouse model and in human HD brain. Finally, compensation of PRMT5 deficiency by ectopic expression of PRMT5/MEP50 complexes, or by the knock-down of H4R3Me2 demethylase JMJD6, reversed the toxic effects of mutant Htt in primary cortical neurons, suggesting that PRMT5 deficiency may mediate, at least in part, HD pathogenesis. These studies revealed a potential new mechanism for disruption of gene expression and RNA processing in HD, involving a loss of normal function of Htt in facilitation of PRMT5, supporting the idea that epigenetic regulation of gene transcription may be involved in HD and highlighting symmetric dimethylation of arginine as potential new therapeutic target.
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