ArticleThe Journal of general physiology2007
Mode switching is the major mechanism of ligand regulation of InsP3 receptor calcium release channels.
Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Modelling ion channels with a view towards identifiability.Bulletin of mathematical biology · 2025Article
- Modeling traveling calcium waves in cellular structures.Journal of computational neuroscience · 2025Article
- A structure-based computational model of IPBiophysical journal · 2024Article
- Conformational motions and ligand-binding underlying gating and regulation in IPNature communications · 2022Article
- Shifts in the selectivity filter dynamics cause modal gating in KNature communications · 2019Article
- All three IPScience signaling · 2018Article
- Cryo-EM reveals ligand induced allostery underlying InsPCell research · 2018Article
- Structural basis for the regulation of inositol trisphosphate receptors by CaNature structural & molecular biology · 2018Article
- Analyzing optical imaging of CaCell calcium · 2017Article
- Alteration of protein function by a silent polymorphism linked to tRNA abundance.PLoS biology · 2017Article
- On the dynamical structure of calcium oscillations.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mode switching of Inositol 1,4,5-trisphosphate receptor channel shapes the Spatiotemporal scales of CaJournal of biological physics · 2016Article
- Emergence of ion channel modal gating from independent subunit kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Modelling modal gating of ion channels with hierarchical Markov models.Proceedings. Mathematical, physical, and engineering sciences · 2016Article
- Modal affinities of endplate acetylcholine receptors caused by loop C mutations.The Journal of general physiology · 2015Article
- Analyzing and Quantifying the Gain-of-Function Enhancement of IP3 Receptor Gating by Familial Alzheimer's Disease-Causing Mutants in Presenilins.PLoS computational biology · 2015Article
- Inositol 1,4,5-trisphosphate receptors in the endoplasmic reticulum: A single-channel point of view.Cell calcium · 2015Review
- Multiscale modelling of saliva secretion.Mathematical biosciences · 2014Article
- Characterization of ryanodine receptor type 1 single channel activity using "on-nucleus" patch clamp.Cell calcium · 2014Article
- A deterministic model predicts the properties of stochastic calcium oscillations in airway smooth muscle cells.PLoS computational biology · 2014Article
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Authors and funding
8 authors.
Funding
Abstract
The inositol 1,4,5-trisphosphate (InsP(3)) receptor (InsP(3)R) plays a critical role in generation of complex Ca(2+) signals in many cell types. In patch clamp recordings of isolated nuclei from insect Sf9 cells, InsP(3)R channels were consistently detected with regulation by cytoplasmic InsP(3) and free Ca(2+) concentrations ([Ca(2+)](i)) very similar to that observed for vertebrate InsP(3)R. Long channel activity durations of the Sf9-InsP(3)R have now enabled identification of a novel aspect of InsP(3)R gating: modal gating. Using a novel algorithm to analyze channel modal gating kinetics, InsP(3)R gating can be separated into three distinct modes: a low activity mode, a fast kinetic mode, and a burst mode with channel open probability (P(o)) within each mode of 0.007 +/- 0.002, 0.24 +/- 0.03, and 0.85 +/- 0.02, respectively. Channels reside in each mode for long periods (tens of opening and closing events), and transitions between modes can be discerned with high resolution (within two channel opening and closing events). Remarkably, regulation of channel gating by [Ca(2+)](i) and [InsP(3)] does not substantially alter channel P(o) within a mode. Instead, [Ca(2+)](i) and [InsP(3)] affect overall channel P(o) primarily by changing the relative probability of the channel being in each mode, especially the high and low P(o) modes. This novel observation therefore reveals modal switching as the major mechanism of physiological regulation of InsP(3)R channel activity, with implications for the kinetics of Ca(2+) release events in cells.
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