The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Calcium–Calmodulin-Dependent Kinase II Modulates Kv4.2 Channel Expression and Upregulates Neuronal A-Type Potassium Currents
Open accessAbstract
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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Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice
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Autophosphorylation at Thr 286 of the α Calcium-Calmodulin Kinase II in LTP and Learning
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An essential role for postsynaptic calmodulin and protein kinase activity in long-term potentiation
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“Moreover, CaMKII has been shown to be necessary and sufficient for LTP induction and necessary for various learning para- digms (Malenka et al., 1989; Malinow et al., 1989; Silva et al., 1992a,b; Pettit et al., 1994; Lledo et al., 1995; Wang and Kelly, 1995; Giese et al., 1998; Hinds et al., 1998).”
BackgroundActivity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system
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Derkach, V., Barria, A., & Soderling, T. R. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.6.3269 · Cited by 842
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Cited by
Chen, X., Yuan, L.-L., Zhao, C., Birnbaum, S. G., Frick, A., Jung, W. E., Schwarz, T. L., Sweatt, J. D., & Johnston, D. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.2667-06.2006 · Cited by 309
Self-citationCalcium/calmodulin-dependent protein kinase II and synaptic plasticity
Colbran, R. J., & Brown, A. M. (2004) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2004.05.008 · Cited by 302
Kim, J., Wei, D., & Hoffman, D. A. (2005) · The Journal of Physiology · doi:10.1113/jphysiol.2005.095042 · Cited by 265
De novo variants in CAMK 2A and CAMK 2B cause neurodevelopmental disorders
Akita, T., Aoto, K., Kato, M., Shiina, M., Mutoh, H., Nakashima, M., Kuki, I., Okazaki, S., Magara, S., Shiihara, T., et al. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.528 · Cited by 87
Siarey, R. J., Kline‐Burgess, A., Cho, M., Balbo, A., Best, T. K., Harashima, C., Klann, E., & Galdzicki, Z. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03971.x · Cited by 86
Metadata
- Authors
- Varga, A. W., Yuan, L.-L., Anderson, A. E., Schrader, L. A., Wu, G.-Y., Gatchel, J. R., Johnston, D., & Sweatt, J. D.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-04-07
- Volume
- 24
- Issue
- 14
- Pages
- 3643-3654
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2141584191
- Cited by
- 168
- References
- 12
- FWCI
- 4.48
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Calcium–Calmodulin-Dependent Kinase II Modulates Kv4.2 Channel Expression and Upregulates Neuronal A-Type Potassium Currents. https://app.cochat.ai/papers/10.1523/jneurosci.0154-04.2004
- The paper
- Varga, A. W., Yuan, L.-L., Anderson, A. E., Schrader, L. A., Wu, G.-Y., Gatchel, J. R., Johnston, D., & Sweatt, J. D. (2004). Calcium–Calmodulin-Dependent Kinase II Modulates Kv4.2 Channel Expression and Upregulates Neuronal A-Type Potassium Currents. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0154-04.2004
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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