ArticleThe Journal of biological chemistry2012
Substrate-selective and calcium-independent activation of CaMKII by α-actinin.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- CaMKIIα inhibition facilitates functional recovery after preterm hypoxic-ischemic brain injury by disrupting microglial GPNMB signaling.Translational pediatrics · 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
- An AlphaFold guided model for the evolution of the CaMKII interactome.bioRxiv : the preprint server for biology · 2025Article
- Structural and functional insights into α-actinin isoforms and their implications in cardiovascular disease.The Journal of general physiology · 2025Review
- GluN2B influences the progression of status epilepticus by modulating calcium ion homeostasis through its interaction with CaMKIIα.Frontiers in pharmacology · 2025Article
- Genomic variations associated with risk and protection against vincristine-induced peripheral neuropathy in pediatric cancer patients.NPJ genomic medicine · 2024Article
- L-Type Calcium Channel Modulates Low-Intensity Pulsed Ultrasound-Induced Excitation in Cultured Hippocampal Neurons.Neuroscience bulletin · 2024Article
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- Molecular basis of interactions between CaMKII and α-actinin-2 that underlie dendritic spine enlargement.eLife · 2023Article
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Global O-GlcNAcylation changes impact desmin phosphorylation and its partition toward cytoskeleton in C2C12 skeletal muscle cells differentiated into myotubes.Scientific reports · 2022Article
- Dendritic Spines in Alzheimer's Disease: How the Actin Cytoskeleton Contributes to Synaptic Failure.International journal of molecular sciences · 2020Review
- Positive Modulation of SK Channel Impedes Neuron-Specific Cytoskeletal Organization and Maturation.Developmental neuroscience · 2020Article
- The Route to 'Chemobrain' - Computational probing of neuronal LTP pathway.Scientific reports · 2019Article
- MAGI1 Mediates eNOS Activation and NO Production in Endothelial Cells in Response to Fluid Shear Stress.Cells · 2019Article
- SK Channel Modulates Synaptic Plasticity by Tuning CaMKIIα/β Dynamics.Frontiers in synaptic neuroscience · 2019Article
- Activated CaMKIIMolecular pharmacology · 2018Article
- Pro-death NMDA receptor signaling is promoted by the GluN2B C-terminus independently of Dapk1.eLife · 2017Article
- Memory Takes Time.Neuron · 2017Review
- Delineating the Common Biological Pathways Perturbed by ASD's Genetic Etiology: Lessons from Network-Based Studies.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Protein-protein interactions are thought to modulate the efficiency and specificity of Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) signaling in specific subcellular compartments. Here we show that the F-actin-binding protein α-actinin targets CaMKIIα to F-actin in cells by binding to the CaMKII regulatory domain, mimicking CaM. The interaction with α-actinin is blocked by CaMKII autophosphorylation at Thr-306, but not by autophosphorylation at Thr-305, whereas autophosphorylation at either site blocks Ca(2+)/CaM binding. The binding of α-actinin to CaMKII is Ca(2+)-independent and activates the phosphorylation of a subset of substrates in vitro. In intact cells, α-actinin selectively stabilizes CaMKII association with GluN2B-containing glutamate receptors and enhances phosphorylation of Ser-1303 in GluN2B, but inhibits CaMKII phosphorylation of Ser-831 in glutamate receptor GluA1 subunits by competing for activation by Ca(2+)/CaM. These data show that Ca(2+)-independent binding of α-actinin to CaMKII differentially modulates the phosphorylation of physiological targets that play key roles in long-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.