ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Autonomous CaMKII requires further stimulation by Ca2+/calmodulin for enhancing synaptic strength.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- CaMKII monomers are sufficient for GluN2B binding, co-condensation, and synaptic potentiation.Molecular cell · 2026Article
- Widely Used CaMKII Regulatory Segment Mutations Cause Tight Actinin Binding and Dendritic Spine Enlargement in Unstimulated Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Aβ impairs the LTP-related movement of endogenous CaMKII but not of exogenous GFP-CaMKII.Molecular biology of the cell · 2025Article
- The neuroprotective γ-hydroxybutyrate analog 3-hydroxycyclopent-1-enecarboxylic acid does not directly affect CaMKIIα autophosphorylation at T286 or binding to GluN2B.Molecular pharmacology · 2025Article
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- The dopamine analogue CA140 alleviates AD pathology, neuroinflammation, and rescues synaptic/cognitive functions by modulating DRD1 signaling or directly binding to Abeta.Journal of neuroinflammation · 2024Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.bioRxiv : the preprint server for biology · 2024Article
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.PloS one · 2024Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Molecular basis of interactions between CaMKII and α-actinin-2 that underlie dendritic spine enlargement.eLife · 2023Article
- Distinct synaptic pools of DAPK1 differentially regulate activity-dependent synaptic CaMKII accumulation.iScience · 2023Article
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- A Modeling and Analysis Study Reveals That CaMKII in Synaptic Plasticity Is a Dominant Affecter in CaM Systems in a T286 Phosphorylation-Dependent Manner.Molecules (Basel, Switzerland) · 2022Article
- Aβ-induced synaptic impairments require CaMKII activity that is stimulated by indirect signaling events.iScience · 2022Article
- Article
- Convergent NMDA receptor-Pannexin1 signaling pathways regulate the interaction of CaMKII with Connexin-36.Communications biology · 2021Article
- CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision.Science advances · 2021Article
- CaMKII versus DAPK1 Binding to GluN2B in Ischemic Neuronal Cell Death after Resuscitation from Cardiac Arrest.Cell reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark feature of Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) is generation of autonomous (Ca(2+)-independent) activity by T286 autophosphorylation. Biochemical studies have shown that "autonomous" CaMKII is ∼5-fold further stimulated by Ca(2+)/CaM, but demonstration of a physiological function for such regulation within cells has remained elusive. In this study, CaMKII-induced enhancement of synaptic strength in rat hippocampal neurons required both autonomous activity and further stimulation. Synaptic strength was decreased by CaMKIIα knockdown and rescued by reexpression, but not by mutants impaired for autonomy (T286A) or binding to NMDA-type glutamate receptor subunit 2B (GluN2B; formerly NR2B; I205K). Full rescue was seen with constitutively autonomous mutants (T286D), but only if they could be further stimulated (additional T305/306A mutation), and not with two other mutations that additionally impair Ca(2+)/CaM binding. Compared to rescue with wild-type CaMKII, the CaM-binding-impaired mutants even had reduced synaptic strength. One of these mutants (T305/306D) mimicked an inhibitory autophosphorylation of CaMKII, whereas the other one (Δstim) abolished CaM binding without introducing charged residues. Inhibitory T305/306 autophosphorylation also reduced GluN2B binding, but this effect was independent of reduced Ca(2+)/CaM binding and was not mimicked by T305/306D mutation. Thus, even autonomous CaMKII activity must be further stimulated by Ca(2+)/CaM for enhancement of synaptic strength.
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