ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Sites and molecular mechanisms of modulation of Na(v)1.2 channels by Fyn tyrosine kinase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. 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, 38 citations in OpenAlex.
- Human microglia-derived proinflammatory cytokines facilitate human retinal ganglion cell development and regeneration.Stem cell reports · 2024Article
- Therapeutic efficacy of voltage-gated sodium channel inhibitors in epilepsy.Acta epileptologica · 2023Review
- Palmitoylation of Voltage-Gated Ion Channels.International journal of molecular sciences · 2022Review
- JAK2 regulates Nav1.6 channel function via FGF14Biochimica et biophysica acta. Molecular cell research · 2020Article
- Regulation of the firing activity by PKA-PKC-Src family kinases in cultured neurons of hypothalamic arcuate nucleus.Journal of neuroscience research · 2020Article
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- c-Src kinase is involved in the tyrosine phosphorylation and activity of SLC11A1 in differentiating macrophages.PloS one · 2018Article
- Src family tyrosine kinase inhibitors suppress Nav1.1 expression in cultured rat spiral ganglion neurons.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2016Article
- An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.Amino acids · 2016Review
- Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels.The Journal of biological chemistry · 2015Article
- SRC tyrosine kinases regulate neuronal differentiation of mouse embryonic stem cells via modulation of voltage-gated sodium channel activity.Neurochemical research · 2015Article
- Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures.The Journal of biological chemistry · 2014Article
- SRC-family tyrosine kinases in oogenesis, oocyte maturation and fertilization: an evolutionary perspective.Advances in experimental medicine and biology · 2014Review
- Localization of sodium channel subtypes in mouse ventricular myocytes using quantitative immunocytochemistry.Journal of molecular and cellular cardiology · 2013Article
- Discovery of a selective NaV1.7 inhibitor from centipede venom with analgesic efficacy exceeding morphine in rodent pain models.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Regulation of voltage-gated sodium current by endogenous Src family kinases in cochlear spiral ganglion neurons in culture.Pflugers Archiv : European journal of physiology · 2012Article
- Receptor protein tyrosine phosphatases are novel components of a polycystin complex.Biochimica et biophysica acta · 2011Article
- Mapping the receptor site for alpha-scorpion toxins on a Na+ channel voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Regulation of sodium channel activity by phosphorylation.Seminars in cell & developmental biology · 2011Review
- Signaling complexes of voltage-gated sodium and calcium channels.Neuroscience letters · 2010Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-gated sodium channels are important targets for modulation of electrical excitability by neurotransmitters and neurotrophins acting through protein phosphorylation. Fast inactivation of Na(V)1.2 channels is regulated via tyrosine phosphorylation by Fyn kinase and dephosphorylation by receptor phosphoprotein tyrosine phosphatase-beta, which are associated in a signaling complex. Here we have identified the amino acid residues on Na(V)1.2 channels that coordinate binding of Fyn kinase and mediate inhibition of sodium currents by enhancing fast inactivation. Fyn kinase binds to a Src homology 3 (SH3)-binding motif in the second half of the intracellular loop connecting domains I and II (L(I-II)) of Na(V)1.2, and mutation of that SH3-binding motif prevents Fyn binding and Fyn enhancement of fast inactivation of sodium currents. Analysis of tyrosine phosphorylation sites by mutagenesis and functional expression revealed a multisite regulatory mechanism. Y66 and Y1893, which are in consensus sequences appropriate for binding to the Fyn SH2 domain after phosphorylation, are both required for optimal binding and regulation by Fyn. Y730, which is located near the SH3-binding motif in L(I-II), and Y1497 and Y1498 in the inactivation gate in L(III-IV), are also required for optimal regulation. Phosphorylation of these sites likely promotes fast inactivation. Fast inactivation of the closely related Na(V)1.1 channels is not modulated by Fyn, and these channels do not contain an SH3-binding motif in L(I-II). Subtype-selective modulation by tyrosine phosphorylation/dephosphorylation provides a mechanism for differential regulation of sodium channels by neurotrophins and tyrosine phosphorylation in unmyelinated axons and dendrites, where Na(V)1.2 channels are expressed in brain neurons.
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