ArticleBiophysical journal2013
The delicate bistability of CaMKII.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics.eLife · 2023Article
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Autoregulation of switching behavior by cellular compartment size.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Interactions between calmodulin and neurogranin govern the dynamics of CaMKII as a leaky integrator.PLoS computational biology · 2020Article
- Article
- Challenges and Opportunities for Therapeutic Targeting of Calmodulin Kinase II in Heart.Frontiers in pharmacology · 2020Review
- From membrane receptors to protein synthesis and actin cytoskeleton: Mechanisms underlying long lasting forms of synaptic plasticity.Seminars in cell & developmental biology · 2019Review
- MCell-R: A Particle-Resolution Network-Free Spatial Modeling Framework.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Active dendrites regulate the spatiotemporal spread of signaling microdomains.PLoS computational biology · 2018Article
- Analog Signaling With the "Digital" Molecular Switch CaMKII.Frontiers in computational neuroscience · 2018Article
- A novel explanation for observed CaMKII dynamics in dendritic spines with added EGTA or BAPTA.Biophysical journal · 2015Article
- In vitro reconstitution of a CaMKII memory switch by an NMDA receptor-derived peptide.Biophysical journal · 2014Article
- First demonstration of bistability in CaMKII, a memory-related kinase.Biophysical journal · 2014Article
- Modeling CaMKII in cardiac physiology: from molecule to tissue.Frontiers in pharmacology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Calcium/calmodulin-dependent protein kinase II (CaMKII) is a synaptic, autophosphorylating kinase that is essential for learning and memory. Previous models have suggested that CaMKII functions as a bistable switch that could be the molecular correlate of long-term memory, but experiments have failed to validate these predictions. These models involved significant approximations to overcome the combinatorial complexity inherent in a multisubunit, multistate system. Here, we develop a stochastic particle-based model of CaMKII activation and dynamics that overcomes combinatorial complexity without significant approximations. We report four major findings. First, the CaMKII model system is never bistable at resting calcium concentrations, which suggests that CaMKII activity does not function as the biochemical switch underlying long-term memory. Second, the steady-state activation curves are either laserlike or steplike. Both are characterized by a well-defined threshold for activation, which suggests that thresholding is a robust feature of this system. Third, transiently activated CaMKII can maintain its activity over the time course of many experiments, and such slow deactivation may account for the few reports of bistability in the literature. And fourth, under in vivo conditions, increases in phosphatase activity can increase CaMKII activity. This is a surprising and counterintuitive effect, as dephosphorylation is generally associated with CaMKII deactivation.
Indexed as
Identifiers
What OpenQuestion holds
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.