ArticleThe Journal of general physiology1999
Agonist-dependent phosphorylation of the inositol 1,4,5-trisphosphate receptor: A possible mechanism for agonist-specific calcium oscillations in pancreatic acinar cells.
Article in The Journal of general physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 100 citations in OpenAlex.
- Pancreatic acinar cell signalling and function exhibit an absolute requirement for activation of GαThe Journal of physiology · 2025Article
- Computational Model of Complex Calcium Dynamics: Store Operated CaCell biochemistry and biophysics · 2025Article
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- Quantifying the dose-dependent impact of intracellular amyloid beta in a mathematical model of calcium regulation in xenopus oocyte.PloS one · 2021Article
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- Computational Model of Ca2+ Wave Propagation in Human Retinal Pigment Epithelial ARPE-19 Cells.PloS one · 2015Article
- Modelling mechanism of calcium oscillations in pancreatic acinar cells.Journal of bioenergetics and biomembranes · 2014Article
- Modelling the transition from simple to complex Ca²⁺ oscillations in pancreatic acinar cells.Journal of biosciences · 2014Article
- Calcium and IP3 dynamics in cardiac myocytes: experimental and computational perspectives and approaches.Frontiers in pharmacology · 2014Review
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- Calcium oscillations.Cold Spring Harbor perspectives in biology · 2011Review
- Regulation of inositol 1,4,5-trisphosphate receptors by cAMP independent of cAMP-dependent protein kinase.The Journal of biological chemistry · 2010Article
- Spatiotemporal organization of Ca dynamics: a modeling-based approach.HFSP journal · 2010Article
- Regulation of inositol 1,4,5-trisphosphate-induced Ca2+ release by reversible phosphorylation and dephosphorylation.Biochimica et biophysica acta · 2009Review
- Inhibition of serine/threonine phosphatase enhances arachidonic acid-induced [Ca2+]i via protein kinase A.American journal of physiology. Cell physiology · 2009Article
- The type 2 inositol (1,4,5)-trisphosphate (InsP3) receptor determines the sensitivity of InsP3-induced Ca2+ release to ATP in pancreatic acinar cells.The Journal of biological chemistry · 2008Article
- Hybrid stochastic and deterministic simulations of calcium blips.Biophysical journal · 2007Article
- Dynamics of a three-variable nonlinear model of vasomotion: comparison of theory and experiment.Biophysical journal · 2007Article
- Modelling calcium microdomains using homogenisation.Journal of theoretical biology · 2007Article
- A buffering SERCA pump in models of calcium dynamics.Biophysical journal · 2006Article
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4 authors at 2 institutions in 1 country.
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Abstract
The properties of inositol 1,4,5-trisphosphate (IP3)-dependent intracellular calcium oscillations in pancreatic acinar cells depend crucially on the agonist used to stimulate them. Acetylcholine or carbachol (CCh) cause high-frequency (10-12-s period) calcium oscillations that are superimposed on a raised baseline, while cholecystokinin (CCK) causes long-period (>100-s period) baseline spiking. We show that physiological concentrations of CCK induce rapid phosphorylation of the IP3 receptor, which is not true of physiological concentrations of CCh. Based on this and other experimental data, we construct a mathematical model of agonist-specific intracellular calcium oscillations in pancreatic acinar cells. Model simulations agree with previous experimental work on the rates of activation and inactivation of the IP3 receptor by calcium (DuFour, J.-F., I.M. Arias, and T.J. Turner. 1997. J. Biol. Chem. 272:2675-2681), and reproduce both short-period, raised baseline oscillations, and long-period baseline spiking. The steady state open probability curve of the model IP3 receptor is an increasing function of calcium concentration, as found for type-III IP3 receptors by Hagar et al. (Hagar, R.E., A.D. Burgstahler, M.H. Nathanson, and B.E. Ehrlich. 1998. Nature. 396:81-84). We use the model to predict the effect of the removal of external calcium, and this prediction is confirmed experimentally. We also predict that, for type-III IP3 receptors, the steady state open probability curve will shift to lower calcium concentrations as the background IP3 concentration increases. We conclude that the differences between CCh- and CCK-induced calcium oscillations in pancreatic acinar cells can be explained by two principal mechanisms: (a) CCK causes more phosphorylation of the IP3 receptor than does CCh, and the phosphorylated receptor cannot pass calcium current; and (b) the rate of calcium ATPase pumping and the rate of calcium influx from the outside the cell are greater in the presence of CCh than in the presence of CCK.
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