ArticleJournal of neurochemistry2010
CaMKII associates with CaV1.2 L-type calcium channels via selected beta subunits to enhance regulatory phosphorylation.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Systematic Review of Calcium Channels and Intracellular Calcium Signaling: Relevance to Pesticide Neurotoxicity.International journal of molecular sciences · 2021Pooled it
- AAV-Delivered RNAi Targeting Mutant LDB3 Prevents and Reverses Myofibrillar Myopathy through Mechanosignaling Restoration.bioRxiv : the preprint server for biology · 2026Article
- The Janus face of CaMKII: from memory consolidation to neurotoxic switch in Alzheimer's disease.Archives of toxicology · 2025Review
- Calmodulin D133H Disrupts CaCells · 2025Article
- CaMKII clusters neuronal LTCCs in biomolecular condensates to gate excitation-transcription coupling.bioRxiv : the preprint server for biology · 2025Article
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- Clustering of CaJournal of neurochemistry · 2023Article
- Compartmentalized cAMP signalling and control of cardiac rhythm.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.Computational and structural biotechnology journal · 2023Review
- Article
- Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing CaInternational journal of molecular sciences · 2021Article
- Article
- Calcium Channel Splice Variants and Their Effects in Brain and Cardiovascular Function.Advances in experimental medicine and biology · 2021Article
- The Interaction between the Drosophila EAG Potassium Channel and the Protein Kinase CaMKII Involves an Extensive Interface at the Active Site of the Kinase.Journal of molecular biology · 2018Article
- Methyl-β-Cyclodextrin Impairs the Phosphorylation of the β₂ Subunit of L-Type Calcium Channels and Cytosolic Calcium Homeostasis in Mature Cerebellar Granule Neurons.International journal of molecular sciences · 2018Article
- The Ras-like GTPase Rem2 is a potent inhibitor of calcium/calmodulin-dependent kinase II activity.The Journal of biological chemistry · 2018Article
- A novel mechanism for CaThe Journal of biological chemistry · 2017Article
- CaMKII-mediated phosphorylation of GluN2B regulates recombinant NMDA receptor currents in a chloride-dependent manner.Molecular and cellular neurosciences · 2017Article
- A Novel HumanThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Calcium/calmodulin-dependent kinase II (CaMKII) facilitates L-type calcium channel (LTCC) activity physiologically, but may exacerbate LTCC-dependent pathophysiology. We previously showed that CaMKII forms stable complexes with voltage-gated calcium channel (VGCC) beta(1b) or beta(2a) subunits, but not with the beta(3) or beta(4) subunits (Grueter et al. 2008). CaMKII-dependent facilitation of Ca(V)1.2 LTCCs requires Thr498 phosphorylation in the beta(2a) subunit (Grueter et al. 2006), but the relationship of this modulation to CaMKII interactions with LTCC subunits is unknown. Here we show that CaMKII co-immunoprecipitates with forebrain LTCCs that contain Ca(V)1.2alpha(1) and beta(1) or beta(2) subunits, but is not detected in LTCC complexes containing beta(4) subunits. CaMKIIalpha can be specifically tethered to the I/II linker of Ca(V)1.2 alpha(1) subunits in vitro by the beta(1b) or beta(2a) subunits. Efficient targeting of CaMKIIalpha to the full-length Ca(V)1.2alpha(1) subunit in transfected HEK293 cells requires CaMKII binding to the beta(2a) subunit. Moreover, disruption of CaMKII binding substantially reduced phosphorylation of beta(2a) at Thr498 within the LTCC complex, without altering overall phosphorylation of Ca(V)1.2alpha(1) and beta subunits. These findings demonstrate a biochemical mechanism underlying LTCC facilitation by CaMKII.
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Registered trials
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