ArticleBiophysical journal2009
CaMKII-induced shift in modal gating explains L-type Ca(2+) current facilitation: a modeling study.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- CaCells · 2024Review
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- Modeling Calcium Cycling in the Heart: Progress, Pitfalls, and Challenges.Biomolecules · 2022Review
- Mathematical model of the ventricular action potential and effects of isoproterenol-induced cardiac hypertrophy in rats.European biophysics journal : EBJ · 2020Article
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Mechanisms of the cyclic nucleotide cross-talk signaling network in cardiac L-type calcium channel regulation.Journal of molecular and cellular cardiology · 2017Article
- Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Circulation research · 2016Article
- Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal.Cardiovascular research · 2016Review
- Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress.Cardiology research and practice · 2016Review
- Interaction between phosphodiesterases in the regulation of the cardiac β-adrenergic pathway.Journal of molecular and cellular cardiology · 2015Article
- Mechanistic Investigation of the Arrhythmogenic Role of Oxidized CaMKII in the Heart.Biophysical journal · 2015Article
- Role of CaMKII in cardiac arrhythmias.Trends in cardiovascular medicine · 2015Review
- Numerical Modeling Calcium and CaMKII Effects in the SA Node.Frontiers in pharmacology · 2014Review
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Modeling CaMKII-mediated regulation of L-type Ca(2+) channels and ryanodine receptors in the heart.Frontiers in pharmacology · 2014Review
- Modal gating of GluN1/GluN2D NMDA receptors.Neuropharmacology · 2013Article
- Pyruvate restores β-adrenergic sensitivity of L-type Ca(2+) channels in failing rat heart: role of protein phosphatase.American journal of physiology. Heart and circulatory physiology · 2013Article
- A Memory Molecule, Ca(2+)/Calmodulin-Dependent Protein Kinase II and Redox Stress; Key Factors for Arrhythmias in a Diseased Heart.Korean circulation journal · 2013Article
- Computational approaches to understand cardiac electrophysiology and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizations.The Journal of physiology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) plays an important role in L-type Ca(2+) channel (LCC) facilitation: the Ca(2+)-dependent augmentation of Ca(2+) current (I(CaL)) exhibited during rapid repeated depolarization. Multiple mechanisms may underlie facilitation, including an increased rate of recovery from Ca(2+)-dependent inactivation and a shift in modal gating distribution from mode 1, the dominant mode of LCC gating, to mode 2, a mode in which openings are prolonged. We hypothesized that the primary mechanism underlying facilitation is the shift in modal gating distribution resulting from CaMKII-mediated LCC phosphorylation. We developed a stochastic model describing the dynamic interactions among CaMKII, LCCs, and phosphatases as a function of dyadic Ca(2+) and calmodulin levels, and we incorporated it into an integrative model of the canine ventricular myocyte. The model reproduces behaviors at physiologic protein levels and allows for dynamic transition between modes, depending on the LCC phosphorylation state. Simulations showed that a CaMKII-dependent shift in LCC distribution toward mode 2 accounted for the I(CaL) positive staircase. Moreover, simulations demonstrated that experimentally observed changes in LCC inactivation and recovery kinetics may arise from modal gating shifts, rather than from changes in intrinsic inactivation properties. The model therefore serves as a powerful tool for interpreting I(CaL) experiments.
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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.