ArticleProceedings of the National Academy of Sciences of the United States of America2008
An allosteric model of calmodulin explains differential activation of PP2B and CaMKII.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. 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 54 papers.
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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
54 citing papers in PubMed, 94 citations in OpenAlex.
- Calmodulin: The Essential Biological Regulator Self-Regulates Its Activity, Structure and Function.Biology · 2026Review
- Obesity-induced oleic acid metabolic dysregulation may exacerbate osteoarthritis through the degradation of SOX9.Cellular and molecular life sciences : CMLS · 2026Article
- Review
- The Cooperation of Neurogranin with Calmodulin Promotes the Treatment of Aging-Related Diseases via Regular Exercise.Molecular neurobiology · 2025Review
- An AlphaFold guided model for the evolution of the CaMKII interactome.bioRxiv : the preprint server for biology · 2025Article
- Long QT syndrome type 3 gain-of-function of NaCommunications biology · 2025Article
- Fitting and comparison of calcium-calmodulin kinetic schemes to a common data set using non-linear mixed effects modelling.PloS one · 2025Article
- Data Hazards as An Ethical Toolkit for Neuroscience.Neuroethics · 2025Article
- DEAD box RNA helicases are pervasive protein kinase interactors and activators.Genome research · 2024Article
- A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics.eLife · 2023Article
- Alzheimer's Disease beyond Calcium Dysregulation: The Complex Interplay between Calmodulin, Calmodulin-Binding Proteins and Amyloid Beta from Disease Onset through Progression.Current issues in molecular biology · 2023Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- A Gating Mutation in Ryanodine Receptor Type 2 Rescues Phenotypes of Alzheimer's Disease Mouse Models by Upregulating Neuronal Autophagy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Binding and Functional Folding (BFF): A Physiological Framework for Studying Biomolecular Interactions and Allostery.Journal of molecular biology · 2022Review
- Behind the scenes: Are latent memories supported by calcium independent plasticity?Hippocampus · 2022Review
- Finite element analysis predicts CaScientific reports · 2021Article
- Incorporation of sensing modalities into de novo designed fluorescence-activating proteins.Nature communications · 2021Article
- Neurogranin, Encoded by the Schizophrenia Risk Gene NRGN, Bidirectionally Modulates Synaptic Plasticity via Calmodulin-Dependent Regulation of the Neuronal Phosphoproteome.Biological psychiatry · 2021Article
- Calmodulin Binding Proteins and Alzheimer's Disease: Biomarkers, Regulatory Enzymes and Receptors That Are Regulated by Calmodulin.International journal of molecular sciences · 2020Review
- Neurogranin stimulates Ca2+/calmodulin-dependent kinase II by suppressing calcineurin activity at specific calcium spike frequencies.PLoS computational biology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calmodulin plays a vital role in mediating bidirectional synaptic plasticity by activating either calcium/calmodulin-dependent protein kinase II (CaMKII) or protein phosphatase 2B (PP2B) at different calcium concentrations. We propose an allosteric model for calmodulin activation, in which binding to calcium facilitates the transition between a low-affinity [tense (T)] and a high-affinity [relaxed (R)] state. The four calcium-binding sites are assumed to be nonidentical. The model is consistent with previously reported experimental data for calcium binding to calmodulin. It also accounts for known properties of calmodulin that have been difficult to model so far, including the activity of nonsaturated forms of calmodulin (we predict the existence of open conformations in the absence of calcium), an increase in calcium affinity once calmodulin is bound to a target, and the differential activation of CaMKII and PP2B depending on calcium concentration.
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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.