ArticleThe Journal of biological chemistry2014
Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Fine mapping and candidate gene analysis of Dravet syndrome modifier loci on mouse chromosomes 7 and 8.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Fine Mapping and Candidate Gene Analysis of Dravet Syndrome Modifier Loci on Mouse Chromosomes 7 and 8.bioRxiv : the preprint server for biology · 2024Article
- Critical Roles of Protein Arginine Methylation in the Central Nervous System.Molecular neurobiology · 2023Review
- Therapeutic efficacy of voltage-gated sodium channel inhibitors in epilepsy.Acta epileptologica · 2023Review
- The Role of Protein Arginine Methyltransferases in DNA Damage Response.International journal of molecular sciences · 2022Review
- Benchmarking the proteomic profile of animal models of mesial temporal epilepsy.Annals of clinical and translational neurology · 2022Article
- Amygdala and anterior cingulate transcriptomes from individuals with bipolar disorder reveal downregulated neuroimmune and synaptic pathways.Nature neuroscience · 2022Article
- Protein arginine methyltransferase 8 modulates mitochondrial bioenergetics and neuroinflammation after hypoxic stress.Journal of neurochemistry · 2021Article
- Activity and Function of the PRMT8 Protein Arginine Methyltransferase in Neurons.Life (Basel, Switzerland) · 2021Review
- Inhibition of Arginine Methylation Impairs Platelet Function.ACS pharmacology & translational science · 2021Article
- [Modulatory effect of 2-arachidonoylglycerol on voltage-gated sodium currents in rat caudate nucleus neurons with kainic acid-induced injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- HCN Channel Phosphorylation Sites Mapped by Mass Spectrometry in Human Epilepsy Patients and in an Animal Model of Temporal Lobe Epilepsy.Neuroscience · 2021Article
- Properties of Calmodulin Binding to NaNeurochemical research · 2021Article
- Palmitic acid methyl ester inhibits cardiac arrest-induced neuroinflammation and mitochondrial dysfunction.Prostaglandins, leukotrienes, and essential fatty acids · 2021Article
- Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function.Molecular neurobiology · 2020Review
- Neuroproteomics in Epilepsy: What Do We Know so Far?Frontiers in molecular neuroscience · 2020Review
- Phosphorylation of the HCN channel auxiliary subunit TRIP8b is altered in an animal model of temporal lobe epilepsy and modulates channel function.The Journal of biological chemistry · 2019Article
- In vivo, in vitro and in silico correlations of four de novo SCN1A missense mutations.PloS one · 2019Article
- The Effect of CaInternational journal of molecular sciences · 2018Article
- Basal Ganglia Neuromodulation Over Multiple Temporal and Structural Scales-Simulations of Direct Pathway MSNs Investigate the Fast Onset of Dopaminergic Effects and Predict the Role of Kv4.2.Frontiers in neural circuits · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated sodium (Nav) channels initiate action potentials in brain neurons and are primary therapeutic targets for anti-epileptic drugs controlling neuronal hyperexcitability in epilepsy. The molecular mechanisms underlying abnormal Nav channel expression, localization, and function during development of epilepsy are poorly understood but can potentially result from altered posttranslational modifications (PTMs). For example, phosphorylation regulates Nav channel gating, and has been proposed to contribute to acquired insensitivity to anti-epileptic drugs exhibited by Nav channels in epileptic neurons. However, whether changes in specific brain Nav channel PTMs occur acutely in response to seizures has not been established. Here, we show changes in PTMs of the major brain Nav channel, Nav1.2, after acute kainate-induced seizures. Mass spectrometry-based proteomic analyses of Nav1.2 purified from the brains of control and seizure animals revealed a significant down-regulation of phosphorylation at nine sites, primarily located in the interdomain I-II linker, the region of Nav1.2 crucial for phosphorylation-dependent regulation of activity. Interestingly, Nav1.2 in the seizure samples contained methylated arginine (MeArg) at three sites. These MeArgs were adjacent to down-regulated sites of phosphorylation, and Nav1.2 methylation increased after seizure. Phosphorylation and MeArg were not found together on the same tryptic peptide, suggesting reciprocal regulation of these two PTMs. Coexpression of Nav1.2 with the primary brain arginine methyltransferase PRMT8 led to a surprising 3-fold increase in Nav1.2 current. Reciprocal regulation of phosphorylation and MeArg of Nav1.2 may underlie changes in neuronal Nav channel function in response to seizures and also contribute to physiological modulation of neuronal excitability.
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