ArticlePhysical biology2012
CaMKII activation and dynamics are independent of the holoenzyme structure: an infinite subunit holoenzyme approximation.
Article in Physical biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 19 citations in OpenAlex.
- Real-time single-molecule imaging of CaMKII-calmodulin interactions.Biophysical journal · 2024Article
- Article
- A multi-state model of the CaMKII dodecamer suggests a role for calmodulin in maintenance of autophosphorylation.PLoS computational biology · 2019Article
- MCell-R: A Particle-Resolution Network-Free Spatial Modeling Framework.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Biophysical attributes that affect CaMKII activation deduced with a novel spatial stochastic simulation approach.PLoS computational biology · 2018Article
- SpringSaLaD: A Spatial, Particle-Based Biochemical Simulation Platform with Excluded Volume.Biophysical journal · 2016Article
- A novel explanation for observed CaMKII dynamics in dendritic spines with added EGTA or BAPTA.Biophysical journal · 2015Article
- Multi-state modeling of biomolecules.PLoS computational biology · 2014Article
- The delicate bistability of CaMKII.Biophysical journal · 2013Article
- Specification, annotation, visualization and simulation of a large rule-based model for ERBB receptor signaling.BMC systems biology · 2012Article
- Rule-based modeling: a computational approach for studying biomolecular site dynamics in cell signaling systems.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The combinatorial explosion produced by the multi-state, multi-subunit character of CaMKII has made analysis and modeling of this key signaling protein a significant challenge. Using rule-based and particle-based approaches, we construct exact models of CaMKII holoenzyme dynamics and study these models as a function of the number of subunits per holoenzyme, N. Without phosphatases the dynamics of activation are independent of the holoenzyme structure unless phosphorylation significantly alters the kinase activity of a subunit. With phosphatases the model is independent of holoenzyme size for N > 6. We introduce an infinite subunit holoenzyme approximation (ISHA), which simplifies the modeling by eliminating the combinatorial complexities encountered in any finite holoenzyme model. The ISHA is an excellent approximation to the full system over a broad range of physiologically relevant parameters. Finally, we demonstrate that the ISHA reproduces the behavior of exact models during synaptic plasticity protocols, which justifies its use as a module in large models of synaptic plasticity.
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.