ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Subunit-specific modulation of KCNQ potassium channels by Src tyrosine kinase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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Who cites it
60 citing papers in PubMed, 102 citations in OpenAlex.
- Inactivation of the Lateral Hypothalamus Attenuates Methamphetamine-Induced Conditioned Place Preference through Regulation of Kcnq3 Expression.International journal of molecular sciences · 2022Article
- Gain of function due to increased opening probability by twoProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Homeostatic regulation of extracellular signal-regulated kinase 1/2 activity and axonal KFrontiers in cellular neuroscience · 2022Article
- KJournal of neurophysiology · 2021Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Article
- Cyclic AMP-Dependent Regulation of Kv7 Voltage-Gated Potassium Channels.Frontiers in physiology · 2020Review
- KFrontiers in cellular neuroscience · 2020Review
- The Role of KFrontiers in physiology · 2020Review
- 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
- The KThe Journal of physiology · 2019Article
- Restoration of Kv7 Channel-Mediated Inhibition Reduces Cued-Reinstatement of Cocaine Seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The Kv7 Channel and Cardiovascular Risk Factors.Frontiers in cardiovascular medicine · 2017Review
- Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling.Molecular and cellular neurosciences · 2016Article
- Rescue of homeostatic regulation of striatal excitability and locomotor activity in a mouse model of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- PP2 prevents β-adrenergic stimulation of cardiac pacemaker activity.Journal of cardiovascular pharmacology · 2014Article
- Differential protein kinase C-dependent modulation of Kv7.4 and Kv7.5 subunits of vascular Kv7 channels.The Journal of biological chemistry · 2014Article
- Kisspeptin activation of TRPC4 channels in female GnRH neurons requires PIP2 depletion and cSrc kinase activation.Endocrinology · 2013Article
- Quantitative properties and receptor reserve of the DAG and PKC branch of G(q)-coupled receptor signaling.The Journal of general physiology · 2013Article
- The neuronal serum- and glucocorticoid-regulated kinase 1.1 reduces neuronal excitability and protects against seizures through upregulation of the M-current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
We studied regulation by c-Src tyrosine kinase (Src) of KCNQ1-5 channels heterologously expressed in Chinese hamster ovary (CHO) cells and of native M current in rat sympathetic neurons. Using whole-cell patch clamp, we found that Src modulates currents from KCNQ3, KCNQ4, and KCNQ5 homomultimers, KCNQ2/3 heteromultimers and native M current, but not currents from KCNQ1 or KCNQ2 homomultimers. Src overexpression had two effects: a decrease of current amplitude (4- to 15-fold for cloned channels and approximately 3-fold for M current) and a slowing of activation kinetics by 2-fold. Both Src actions were mostly reversed by bath application of the Src inhibitors erbstatin (20 microm) and PP2 (200 nm), and mimicked by the tyrosine phosphatase inhibitor sodium vanadate (100 microm). Immunoprecipitation and immunoblot analysis showed Src-dependent phosphotyrosine signals associated with KCNQ3, KCNQ4, and KCNQ5 but not with KCNQ1 or KCNQ2 that may be tyrosine phosphorylation of the channel subunits. Expression of a dominant negative Src that cannot phosphorylate substrates had no effect on the current and did not induce phosphotyrosine signals associated with KCNQ3-5 subunits, further indicating that Src actions on KCNQ currents are mediated by tyrosine phosphorylation. Immunostaining and confocal analysis showed no effect of Src overexpression on the abundance of KCNQ3 protein in CHO cells. Finally, experiments using cloned KCNQ2/3 channels, Src and M(1) muscarinic receptors, and sympathetic neurons demonstrated that the actions on KCNQ channels by Src and by muscarinic agonists use distinct mechanisms.
Indexed as
Identifiers
12514204PMC6742119W2145102240What OpenQuestion holds
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.