ArticleeLife2016
Protein arginine methylation facilitates KCNQ channel-PIP2 interaction leading to seizure suppression.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Role of Glycerophospholipid Metabolism in Epilepsy.Current neuropharmacology · 2026Review
- Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.Cellular and molecular neurobiology · 2025Review
- Article
- Functional Implications of Protein Arginine Methyltransferases (PRMTs) in Neurodegenerative Diseases.Biology · 2023Review
- Involvement of CaCellular and molecular neurobiology · 2023Article
- HumanJournal of neurophysiology · 2022Article
- Modulation of IJournal of cellular physiology · 2022Article
- Review
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- Structure, Activity, and Function of PRMT1.Life (Basel, Switzerland) · 2021Review
- Protein arginine methylation: from enigmatic functions to therapeutic targeting.Nature reviews. Drug discovery · 2021Review
- Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function.Molecular neurobiology · 2020Review
- TwoFrontiers in physiology · 2020Article
- Kv7 Channels in Lung Diseases.Frontiers in physiology · 2020Review
- An improved protein lipid overlay assay for studying lipid-protein interactions.Plant methods · 2020Article
- Skeletal muscle-specific Prmt1 deletion causes muscle atrophy via deregulation of the PRMT6-FOXO3 axis.Autophagy · 2019Article
- Gq-Coupled Muscarinic Receptor Enhancement of KCNQ2/3 Channels and Activation of TRPC Channels in Multimodal Control of Excitability in Dentate Gyrus Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- PRMT1 Deficiency in Mouse Juvenile Heart Induces Dilated Cardiomyopathy and Reveals Cryptic Alternative Splicing Products.iScience · 2018Article
- Reduced axonal surface expression and phosphoinositide sensitivity in KNeurobiology of disease · 2018Article
- Activation of ROP6 GTPase by Phosphatidylglycerol in Arabidopsis.Frontiers in plant science · 2018Article
Corrections and comments
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Authors and funding
22 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KCNQ channels are critical determinants of neuronal excitability, thus emerging as a novel target of anti-epileptic drugs. To date, the mechanisms of KCNQ channel modulation have been mostly characterized to be inhibitory via Gq-coupled receptors, Ca(2+)/CaM, and protein kinase C. Here we demonstrate that methylation of KCNQ by protein arginine methyltransferase 1 (Prmt1) positively regulates KCNQ channel activity, thereby preventing neuronal hyperexcitability. Prmt1+/- mice exhibit epileptic seizures. Methylation of KCNQ2 channels at 4 arginine residues by Prmt1 enhances PIP2 binding, and Prmt1 depletion lowers PIP2 affinity of KCNQ2 channels and thereby the channel activities. Consistently, exogenous PIP2 addition to Prmt1+/- neurons restores KCNQ currents and neuronal excitability to the WT level. Collectively, we propose that Prmt1-dependent facilitation of KCNQ-PIP2 interaction underlies the positive regulation of KCNQ activity by arginine methylation, which may serve as a key target for prevention of neuronal hyperexcitability and seizures.
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Registered trials
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.