ArticleCell2011
A mechanism for tunable autoinhibition in the structure of a human Ca2+/calmodulin- dependent kinase II holoenzyme.
Article in Cell, 2011. 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 162 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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Who cites it
162 citing papers in PubMed.
- CaMKIIα holoenzymes self-organize into chain-like mesoscale clusters.Science advances · 2026Article
- Transcription Factor HOXC11 Drives Colorectal Cancer Progression and Metastasis via CAMK2A-Dependent CXCL5 Upregulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Bacterial ubiquitin ligase engineered for small molecule and protein target identification.The EMBO journal · 2026Article
- Calcium signaling and postsynaptic density dynamics: the roles of calmodulin in synaptic protein regulation.Frontiers in molecular neuroscience · 2026Review
- Structural dynamics of mixed-subunit CaMKIIα/β heterododecamers filmed by high-speed AFM.Nature communications · 2025Article
- 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
- A domain-swapped CaMKII conformation facilitates linker-mediated allosteric regulation.Nature communications · 2025Article
- An AlphaFold guided model for the evolution of the CaMKII interactome.bioRxiv : the preprint server for biology · 2025Article
- Sublytic Activity of a Pore-Forming Protein From Commensal Bacteria Causes Epigenetic Modulation of Tumour-Affiliated Protein Expression.Journal of extracellular vesicles · 2025Article
- CaInflammation and regeneration · 2025Review
- Phase Separation Clustering of Poly Ubiquitin Cargos on Ternary Mixture Lipid Membranes by Synthetically Cross-Linked Ubiquitin Binder Peptides.Biochemistry · 2025Article
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- Oxidation of CaMKIIα cysteines inhibits autonomous activation induced by phosphorylation.Archives of biochemistry and biophysics · 2025Article
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- A spatial model of autophosphorylation of CaMKII predicts that the lifetime of phospho-CaMKII after induction of synaptic plasticity is greatly prolonged by CaM-trapping.Frontiers in synaptic neuroscience · 2025Article
- A spatial model of autophosphorylation of CabioRxiv : the preprint server for biology · 2024Article
- Site-specific incorporation ofCommunications biology · 2024Article
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- Exploring Metabolic Mechanisms in Calcific Tendinopathy and Shoulder Arthrofibrosis: Insights and Therapeutic Implications.Journal of clinical medicine · 2024Review
102 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Calcium/calmodulin-dependent kinase II (CaMKII) forms a highly conserved dodecameric assembly that is sensitive to the frequency of calcium pulse trains. Neither the structure of the dodecameric assembly nor how it regulates CaMKII are known. We present the crystal structure of an autoinhibited full-length human CaMKII holoenzyme, revealing an unexpected compact arrangement of kinase domains docked against a central hub, with the calmodulin-binding sites completely inaccessible. We show that this compact docking is important for the autoinhibition of the kinase domains and for setting the calcium response of the holoenzyme. Comparison of CaMKII isoforms, which differ in the length of the linker between the kinase domain and the hub, demonstrates that these interactions can be strengthened or weakened by changes in linker length. This equilibrium between autoinhibited states provides a simple mechanism for tuning the calcium response without changes in either the hub or the kinase domains.
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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.