ArticleBiophysical journal1999
Determination of time-dependent inositol-1,4,5-trisphosphate concentrations during calcium release in a smooth muscle cell.
Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 64 citations in OpenAlex.
- A 3D-1D-0D multiscale model of the neuro-glial-vascular unit for synaptic and vascular dynamics in the dorsal vagal complex.Journal of mathematical biology · 2025Article
- The role of astrocytic calcium and TRPV4 channels in neurovascular coupling.Journal of computational neuroscience · 2018Article
- Article
- Cyclic AMP Recruits a Discrete Intracellular CaCell reports · 2017Article
- Modelling the vascular response to sympathetic postganglionic nerve activity.Journal of theoretical biology · 2015Article
- Computational Model of Ca2+ Wave Propagation in Human Retinal Pigment Epithelial ARPE-19 Cells.PloS one · 2015Article
- Mast cell-nerve cell interaction at acupoint: modeling mechanotransduction pathway induced by acupuncture.International journal of biological sciences · 2014Article
- A positive feedback cell signaling nucleation model of astrocyte dynamics.Frontiers in neuroengineering · 2013Article
- Article
- Modeling Ca2+ signaling in the microcirculation: intercellular communication and vasoreactivity.Critical reviews in biomedical engineering · 2011Review
- A mathematical analysis of agonist- and KCl-induced Ca(2+) oscillations in mouse airway smooth muscle cells.Biophysical journal · 2010Article
- Kinetics of PIP2 metabolism and KCNQ2/3 channel regulation studied with a voltage-sensitive phosphatase in living cells.The Journal of general physiology · 2010Article
- Use of virtual cell in studies of cellular dynamics.International review of cell and molecular biology · 2010Review
- Systemic Analysis of Tumor Cell-Induced Endothelial Calcium Signaling and Junction Disassembly.Cellular and molecular bioengineering · 2009Article
- Where does all the PIP2 come from?The Journal of physiology · 2007Article
- Compartment-specific feedback loop and regulated trafficking can result in sustained activation of Ras at the Golgi.Biophysical journal · 2007Article
- A quantitative model of purinergic junctional transmission of calcium waves in astrocyte networks.Biophysical journal · 2005Article
- A signal transduction pathway model prototype II: Application to Ca2+-calmodulin signaling and myosin light chain phosphorylation.Biophysical journal · 2004Article
- A signal transduction pathway model prototype I: From agonist to cellular endpoint.Biophysical journal · 2004Article
- Kinetic analysis of receptor-activated phosphoinositide turnover.The Journal of cell biology · 2003Article
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
Abstract
The level of [InsP3]cyt required for calcium release in A7r5 cells, a smooth muscle cell line, was determined by a new set of procedures using quantitative confocal microscopy to measure release of InsP3 from cells microinjected with caged InsP3. From these experiments, the [InsP3]cyt required to evoke a half-maximal calcium response is 100 nM. Experiments with caged glycerophosphoryl-myo-inositol 4, 5-bisphosphate (GPIP2), a slowly metabolized analogue of InsP3, gave a much slower recovery and a half-maximal response of an order of magnitude greater than InsP3. Experimental data and highly constrained variables were used to construct a mathematical model of the InsP3-dependent [Ca2+]cyt changes; the resulting simulations show high fidelity to experiment. Among the elements considered in constructing this model were the mechanism of the InsP3-receptor, InsP3 degradation, calcium buffering in the cytosol, and refilling of the ER stores via sarcoplasmic endoplasmic reticulum ATPase (SERCA) pumps. The model predicts a time constant of 0.8 s for InsP3 degradation and 13 s for GPIP2. InsP3 degradation was found to be a prerequisite for [Ca2+]cyt recovery to baseline levels and is therefore critical to the pattern of the overall [Ca2+]cyt signal. Analysis of the features of this model provides insights into the individual factors controlling the amplitude and shape of the InsP3-mediated calcium signal.
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.