ArticleBiophysical journal2008
Modeling Ca2+ feedback on a single inositol 1,4,5-trisphosphate receptor and its modulation by Ca2+ buffers.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Close agreement between deterministic versus stochastic modeling of first-passage time to vesicle fusion.Biophysical journal · 2022Article
- IPeLife · 2020Article
- Simulation of calcium signaling in fine astrocytic processes: Effect of spatial properties on spontaneous activity.PLoS computational biology · 2019Article
- Emergence of ion channel modal gating from independent subunit kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Inositol 1,4,5-trisphosphate receptors in the endoplasmic reticulum: A single-channel point of view.Cell calcium · 2015Review
- Exact stochastic simulation of a calcium microdomain reveals the impact of Ca²⁺ fluctuations on IP₃R gating.Biophysical journal · 2015Article
- The influence of Ca²⁺ buffers on free [Ca²⁺] fluctuations and the effective volume of Ca²⁺ microdomains.Biophysical journal · 2014Article
- Frequency and relative prevalence of calcium blips and puffs in a model of small IP₃R clusters.Biophysical journal · 2014Article
- Stochastic contribution for the coding of agonist induced calcium oscillation in hepatocytes.European biophysics journal : EBJ · 2013Article
- Developmental profile of localized spontaneous Ca(2+) release events in the dendrites of rat hippocampal pyramidal neurons.Cell calcium · 2012Article
- Multi-scale data-driven modeling and observation of calcium puffs.Cell calcium · 2012Article
- Termination of Ca²+ release for clustered IP₃R channels.PLoS computational biology · 2012Article
- Understanding calcium waves and sparks in central neurons.Nature reviews. Neuroscience · 2012Review
- Unitary Ca(2+) current through recombinant type 3 InsP(3) receptor channels under physiological ionic conditions.The Journal of general physiology · 2010Article
- Calcium signals driven by single channel noise.PLoS computational biology · 2010Article
- Calcium domains around single and clustered IP3 receptors and their modulation by buffers.Biophysical journal · 2010Article
- Stochastic simulation of calcium microdomains in the vicinity of an L-type calcium channel.European biophysics journal : EBJ · 2010Article
- Intra-cluster percolation of calcium signals.PloS one · 2010Article
- A simple sequential-binding model for calcium puffs.Chaos (Woodbury, N.Y.) · 2009Article
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 2 institutions in 2 countries.
Funding
Abstract
The inositol 1,4,5-trisphosphate receptor/channel (IP(3)R) is a major regulator of intracellular Ca(2+) signaling, and liberates Ca(2+) ions from the endoplasmic reticulum in response to binding at cytosolic sites for both IP(3) and Ca(2+). Although the steady-state gating properties of the IP(3)R have been extensively studied and modeled under conditions of fixed [IP(3)] and [Ca(2+)], little is known about how Ca(2+) flux through a channel may modulate the gating of that same channel by feedback onto activating and inhibitory Ca(2+) binding sites. We thus simulated the dynamics of Ca(2+) self-feedback on monomeric and tetrameric IP(3)R models. A major conclusion is that self-activation depends crucially on stationary cytosolic Ca(2+) buffers that slow the collapse of the local [Ca(2+)] microdomain after closure. This promotes burst-like reopenings by the rebinding of Ca(2+) to the activating site; whereas inhibitory actions are substantially independent of stationary buffers but are strongly dependent on the location of the inhibitory Ca(2+) binding site on the IP(3)R in relation to the channel pore.
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.