ArticlePloS one2012
Calcium input frequency, duration and amplitude differentially modulate the relative activation of calcineurin and CaMKII.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 125 citations in OpenAlex.
- Calmodulin: The Essential Biological Regulator Self-Regulates Its Activity, Structure and Function.Biology · 2026Review
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- The role of calcium homeostasis dysregulation in allergic rhinitis.Frontiers in immunology · 2026Review
- Rules of life at the interface of calcium signaling and mechanobiology.APL bioengineering · 2025Review
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 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
- Hybrid CMOS-Memristor synapse circuits for implementing Ca ion-based plasticity model.Scientific reports · 2024Article
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Targeting EB3-IPAmerican journal of respiratory cell and molecular biology · 2023Article
- Numerous Trigger-like Interactions of Kinases/Protein Phosphatases in Human Skeletal Muscles Can Underlie Transient Processes in Activation of Signaling Pathways during Exercise.International journal of molecular sciences · 2023Review
- 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
- Article
- Piezo1 is the cardiac mechanosensor that initiates the cardiomyocyte hypertrophic response to pressure overload in adult mice.Nature cardiovascular research · 2022Article
- Behind the scenes: Are latent memories supported by calcium independent plasticity?Hippocampus · 2022Review
- Calcineurin in the heart: New horizons for an old friend.Cellular signalling · 2021Review
- Electroacupuncture Reverses CUMS-Induced Depression-Like Behaviors and LTP Impairment in Hippocampus by Downregulating NR2B and CaMK II Expression.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Effects of datumetine on hippocampal NMDAR activity.Toxicology reports · 2021Article
- Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NMDA receptor dependent long-term potentiation (LTP) and long-term depression (LTD) are two prominent forms of synaptic plasticity, both of which are triggered by post-synaptic calcium elevation. To understand how calcium selectively stimulates two opposing processes, we developed a detailed computational model and performed simulations with different calcium input frequencies, amplitudes, and durations. We show that with a total amount of calcium ions kept constant, high frequencies of calcium pulses stimulate calmodulin more efficiently. Calcium input activates both calcineurin and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) at all frequencies, but increased frequencies shift the relative activation from calcineurin to CaMKII. Irrespective of amplitude and duration of the inputs, the total amount of calcium ions injected adjusts the sensitivity of the system to calcium input frequencies. At a given frequency, the quantity of CaMKII activated is proportional to the total amount of calcium. Thus, an input of a small amount of calcium at high frequencies can induce the same activation of CaMKII as a larger amount, at lower frequencies. Finally, the extent of activation of CaMKII signals with high calcium frequency is further controlled by other factors, including the availability of calmodulin, and by the potency of phosphatase inhibitors.
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.