ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Calcium-calmodulin-dependent kinase II modulates Kv4.2 channel expression and upregulates neuronal A-type potassium currents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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76 citing papers in PubMed, 169 citations in OpenAlex.
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- Subcellular localization of hippocampal ryanodine receptor 2 and its role in neuronal excitability and memory.Communications biology · 2022Article
- R-type voltage-gated CaCell reports · 2022Article
- Calcium/calmodulin-dependent protein kinase II associates with the KFrontiers in neuroanatomy · 2022Article
- Calbindin regulates Kv4.1 trafficking and excitability in dentate granule cells via CaMKII-dependent phosphorylation.Experimental & molecular medicine · 2021Article
- Paradoxical relationships between active transport and global protein distributions in neurons.Biophysical journal · 2021Article
- Limiting RyR2 Open Time Prevents Alzheimer's Disease-Related Neuronal Hyperactivity and Memory Loss but Not β-Amyloid Accumulation.Cell reports · 2020Article
- Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A novel bungarotoxin binding site-tagged construct reveals MAPK-dependent Kv4.2 trafficking.Molecular and cellular neurosciences · 2019Article
- GSK3β Modulates Timing-Dependent Long-Term Depression Through Direct Phosphorylation of Kv4.2 Channels.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Transient Potassium Channels: Therapeutic Targets for Brain Disorders.Frontiers in cellular neuroscience · 2019Review
- The Sigma-1 Receptor: When Adaptive Regulation of Cell Electrical Activity Contributes to Stimulant Addiction and Cancer.Frontiers in neuroscience · 2019Review
- Autophosphorylated CaMKII Facilitates Spike Propagation in Rat Optic Nerve.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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- Potent block of potassium channels by MEK inhibitor U0126 in primary cultures and brain slices.Scientific reports · 2018Article
- Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-calmodulin-dependent kinase II (CaMKII) has a long history of involvement in synaptic plasticity, yet little focus has been given to potassium channels as CaMKII targets despite their importance in repolarizing EPSPs and action potentials and regulating neuronal membrane excitability. We now show that Kv4.2 acts as a substrate for CaMKII in vitro and have identified CaMKII phosphorylation sites as Ser438 and Ser459. To test whether CaMKII phosphorylation of Kv4.2 affects channel biophysics, we expressed wild-type or mutant Kv4.2 and the K(+) channel interacting protein, KChIP3, with or without a constitutively active form of CaMKII in Xenopus oocytes and measured the voltage dependence of activation and inactivation in each of these conditions. CaMKII phosphorylation had no effect on channel biophysical properties. However, we found that levels of Kv4.2 protein are increased with CaMKII phosphorylation in transfected COS cells, an effect attributable to direct channel phosphorylation based on site-directed mutagenesis studies. We also obtained corroborating physiological data showing increased surface A-type channel expression as revealed by increases in peak K(+) current amplitudes with CaMKII phosphorylation. Furthermore, endogenous A-currents in hippocampal pyramidal neurons were increased in amplitude after introduction of constitutively active CaMKII, which results in a decrease in neuronal excitability in response to current injections. Thus CaMKII can directly modulate neuronal excitability by increasing cell-surface expression of A-type K(+) channels.
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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.