ArticleNeuron2015
A Temporary Gating of Actin Remodeling during Synaptic Plasticity Consists of the Interplay between the Kinase and Structural Functions of CaMKII.
Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 papers.
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
82 citing papers in PubMed, 147 citations in OpenAlex.
- Resveratrol as a modulator of synaptic plasticity: molecular mechanisms and future therapeutic perspectives.Molecular biology reports · 2026Review
- CaMKIIα holoenzymes self-organize into chain-like mesoscale clusters.Science advances · 2026Article
- Generalization of negative memories drives the development of psychological distress-related behaviors.Innovation (Cambridge (Mass.)) · 2026Article
- The conserved fibroblast growth factor receptor-based signaling is required for dendrite regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- Synaptic spine head morphodynamics from graph grammar rules for actin dynamics.bioRxiv : the preprint server for biology · 2026Article
- Structural dynamics of mixed-subunit CaMKIIα/β heterododecamers filmed by high-speed AFM.Nature communications · 2025Article
- Epigenetic Mechanisms Shaping Spine Regulation: Unveiling the Role of Cytoskeletal Dynamics and Localized Protein Synthesis.Molecular neurobiology · 2025Review
- A domain-swapped CaMKII conformation facilitates linker-mediated allosteric regulation.Nature communications · 2025Article
- Role of LIMK1-cofilin-actin axis in dendritic spine dynamics in Alzheimer's disease.Cell death & disease · 2025Review
- Article
- Synaptic Plasticity Linked to Ionotropic Glutamate Receptors After Nicotine Exposure.Current neuropharmacology · 2025Review
- Tropisetron, an Antiemetic Drug, Exerts an Anti-Epileptic Effect Through the Activation of α7nAChRs in a Rat Model of Temporal Lobe Epilepsy.CNS neuroscience & therapeutics · 2024Article
- Chromophore-Assisted Light Inactivation for Protein Degradation and Its Application in Biomedicine.Bioengineering (Basel, Switzerland) · 2024Review
- Electro-Metabolic Coupling of Cumulus-Oocyte Complex.International journal of molecular sciences · 2024Review
- Real-time single-molecule imaging of CaMKII-calmodulin interactions.Biophysical journal · 2024Article
- Calcium-Associated Proteins in Neuroregeneration.Biomolecules · 2024Review
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Two-Photon FRET/FLIM Imaging of Cerebral Neurons.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
Abstract
The structural modification of dendritic spines plays a critical role in synaptic plasticity. CaMKII is a pivotal molecule involved in this process through both kinase-dependent and independent structural functions, but the respective contributions of these two functions to the synaptic plasticity remain unclear. We demonstrate that the transient interplay between the kinase and structural functions of CaMKII during the induction of synaptic plasticity temporally gates the activity-dependent modification of the actin cytoskeleton. Inactive CaMKII binds F-actin, thereby limiting access of actin-regulating proteins to F-actin and stabilizing spine structure. CaMKII-activating stimuli trigger dissociation of CaMKII from F-actin through specific autophosphorylation reactions within the F-actin binding region and permits F-actin remodeling by regulatory proteins followed by reassociation and restabilization. Blocking the autophosphorylation impairs both functional and structural plasticity without affecting kinase activity. These results underpin the importance of the interplay between the kinase and structural functions of CaMKII in defining a time window permissive for 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.