ArticleThe Journal of biological chemistry2013
Ca2+-independent activation of Ca2+/calmodulin-dependent protein kinase II bound to the C-terminal domain of CaV2.1 calcium channels.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Exogenous 3-Iodothyronamine (TLife (Basel, Switzerland) · 2022Article
- A survey of protein interactions and posttranslational modifications that influence the polyglutamine diseases.Frontiers in molecular neuroscience · 2022Review
- Neurotransmitter Release Site Replenishment and Presynaptic Plasticity.International journal of molecular sciences · 2020Review
- Integrated Proteogenomic Characterization across Major Histological Types of Pediatric Brain Cancer.Cell · 2020Article
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- The Ras-like GTPase Rem2 is a potent inhibitor of calcium/calmodulin-dependent kinase II activity.The Journal of biological chemistry · 2018Article
- Prevention of long-term memory loss after retrieval by an endogenous CaMKII inhibitor.Scientific reports · 2017Article
- Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Inhibition of cardiac CaMKII to cure heart failure: step by step towards translation?Basic research in cardiology · 2016Article
- Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016Review
- Optimization of neuronal cultures from rat superior cervical ganglia for dual patch recording.Scientific reports · 2015Article
- Neural activity selects myosin IIB and VI with a specific time window in distinct dynamin isoform-mediated synaptic vesicle reuse pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Modulation of CaV2.1 channels by neuronal calcium sensor-1 induces short-term synaptic facilitation.Molecular and cellular neurosciences · 2014Article
- CaMKII inhibitors: from research tools to therapeutic agents.Frontiers in pharmacology · 2014Review
- The amino-terminus of high voltage activated calcium channels: CaM you or can't you?Channels (Austin, Tex.) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) forms a major component of the postsynaptic density where its functions in synaptic plasticity are well established, but its presynaptic actions are poorly defined. Here we show that CaMKII binds directly to the C-terminal domain of Ca(V)2.1 channels. Binding is enhanced by autophosphorylation, and the kinase-channel signaling complex persists after dephosphorylation and removal of the Ca(2+)/CaM stimulus. Autophosphorylated CaMKII can bind the Ca(V)2.1 channel and synapsin-1 simultaneously. CaMKII binding to Ca(V)2.1 channels induces Ca(2+)-independent activity of the kinase, which phosphorylates the enzyme itself as well as the neuronal substrate synapsin-1. Facilitation and inactivation of Ca(V)2.1 channels by binding of Ca(2+)/CaM mediates short term synaptic plasticity in transfected superior cervical ganglion neurons, and these regulatory effects are prevented by a competing peptide and the endogenous brain inhibitor CaMKIIN, which blocks binding of CaMKII to Ca(V)2.1 channels. These results define the functional properties of a signaling complex of CaMKII and Ca(V)2.1 channels in which both binding partners are persistently activated by their association, and they further suggest that this complex is important in presynaptic terminals in regulating protein phosphorylation and short term synaptic plasticity.
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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.