Evidence map›Paper›PMID 10352035›Full record

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.

A P LeBeau, D I Yule, G E Groblewski, J Sneyd

Open access · bronzeAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Modelling mechanism of calcium oscillations in pancreatic acinar cells.Journal of bioenergetics and biomembranes · 2014
    Article
  8. Article
  9. Review
  10. Article
  11. Calcium oscillations.Cold Spring Harbor perspectives in biology · 2011
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Modelling calcium microdomains using homogenisation.Journal of theoretical biology · 2007
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

A P LeBeauMathematical Research Branch, National Institutes of Health, Bethesda, Maryland, USA.
D I Yule
G E Groblewski
J Sneyd
University of Michigan–Ann Arbor · USNational Institutes of Health · US

Funding

PANCREATIC SECRETION--G PROTEIN MEDIATED CA++ SIGNALINGR01DK054568 · NIDDK · UNIVERSITY OF ROCHESTER · PI YULE, DAVID I · 1998 to 2012
$3.1M
MECHANISMS OF INTERCELLULAR CALCIUM WAVESR01GM056126 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SNEYD, A. JAMES R. · 1997 to 1999
–
NIDDK NIH HHS R01 DK054568NIDDK NIH HHS R01 DK54568NIGMS NIH HHS R01 GM56126
6 · The paper itself

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.

Indexed as

Models, ChemicalAcetylcholineAnimalsCalciumCalcium ChannelsCarbacholCholecystokininCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme InhibitorsIndolesInositol 1,4,5-Trisphosphate ReceptorsIon Channel GatingMalePancreasParasympathomimetics8-((4-chlorophenyl)thio)cyclic-3',5'-AMPAcetylcholineCalciumCalcium ChannelsCarbacholCholecystokininCyclic AMPCyclic AMP-Dependent Protein Kinasescyclopiazonic acidEnzyme InhibitorsIndolesInositol 1,4,5-Trisphosphate ReceptorsParasympathomimeticsReceptors, Cytoplasmic and NuclearThionucleotidesVasodilator Agents

Identifiers

PMID10352035
PMCPMC2225599
OpenAlexW2125597366

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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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.