ArticleThe Journal of biological chemistry2000
TrkB activation by brain-derived neurotrophic factor inhibits the G protein-gated inward rectifier Kir3 by tyrosine phosphorylation of the channel.
Article in The Journal of biological chemistry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 69 citations in OpenAlex.
- Intravenous administration of auto serum-expanded autologous mesenchymal stem cells in stroke.Brain : a journal of neurology · 2011Trial
- Sortilin and L-type Calcium Channels May be Involved in the Unusual Mechanism of proBDNF Signaling in Regenerating Mouse Neuromuscular Junctions.Neurochemical research · 2025Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses.Frontiers in cellular neuroscience · 2022Article
- BDNF downregulates β-adrenergic receptor-mediated hypotensive mechanisms in the paraventricular nucleus of the hypothalamus.American journal of physiology. Heart and circulatory physiology · 2019Article
- Possible Molecular Mediators Involved and Mechanistic Insight into Fibromyalgia and Associated Co-morbidities.Neurochemical research · 2019Review
- The ICl,swell inhibitor DCPIB blocks Kir channels that possess weak affinity for PIP2.Pflugers Archiv : European journal of physiology · 2016Article
- Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.Frontiers in cellular neuroscience · 2016Review
- Kappa Opioid Receptor-Induced Aversion Requires p38 MAPK Activation in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels.The Journal of biological chemistry · 2015Article
- Structural elements in the Girk1 subunit that potentiate G protein-gated potassium channel activity.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Repeated stress dysregulates κ-opioid receptor signaling in the dorsal raphe through a p38α MAPK-dependent mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Functional consequences of the interactions among the neural cell adhesion molecule NCAM, the receptor tyrosine kinase TrkB, and the inwardly rectifying K+ channel KIR3.3.The Journal of biological chemistry · 2010Article
- Tyrosine phosphorylation of Kir3 following kappa-opioid receptor activation of p38 MAPK causes heterologous desensitization.The Journal of biological chemistry · 2009Article
- Regulation of wild-type and mutant KCNQ1/KCNE1 channels by tyrosine kinase.Pflugers Archiv : European journal of physiology · 2009Article
- Brain-derived neurotrophic factor enhances the excitability of rat sensory neurons through activation of the p75 neurotrophin receptor and the sphingomyelin pathway.The Journal of physiology · 2008Article
- Diverse Kir modulators act in close proximity to residues implicated in phosphoinositide binding.The Journal of physiology · 2007Review
- Article
- Tyrosine phosphorylation of K(ir)3.1 in spinal cord is induced by acute inflammation, chronic neuropathic pain, and behavioral stress.The Journal of biological chemistry · 2005Article
- Receptor-induced depletion of phosphatidylinositol 4,5-bisphosphate inhibits inwardly rectifying K+ channels in a receptor-specific manner.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
G protein-activated inwardly rectifying potassium channels (Kir3) are widely expressed throughout the brain, and regulation of their activity modifies neuronal excitability and synaptic transmission. In this study, we show that the neurotrophin brain-derived neurotrophic factor (BDNF), through activation of TrkB receptors, strongly inhibited the basal activity of Kir3. This inhibition was subunit dependent as functional homomeric channels of either Kir3.1 or Kir3.4 were significantly inhibited, whereas homomeric channels composed of Kir3.2 were insensitive. The general tyrosine kinase inhibitors genistein, Gö 6976, and K252a but not the serine/threonine kinase inhibitor staurosporine blocked the BDNF-induced inhibition of the channel. BDNF was also found to directly stimulate channel phosphorylation because Kir3.1 immunoprecipitated from BDNF-stimulated cells showed enhanced labeling by anti-phosphotyrosine-specific antibodies. The BDNF effect required specific tyrosine residues in the amino terminus of Kir3.1 and Kir3.4 channels. Mutations of either Tyr-12, Tyr-67, or both in Kir3.1 or mutation of either Tyr-32, Tyr-53, or both of Kir3. 4 channels to phenylalanine significantly blocked the BDNF-induced inhibition. The insensitive Kir3.2 was made sensitive to BDNF by adding a tyrosine (D41Y) and a lysine (P32K) upstream to generate a phosphorylation site motif analogous to that present in Kir3.4. These results suggest that neurotrophin activation of TrkB receptors may physiologically control neuronal excitability by direct tyrosine phosphorylation of the Kir3.1 and Kir3.4 subunits of G protein-gated inwardly rectifying potassium channels.
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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.