ArticleThe Biochemical journal1996
Synergistic effects of inositol 1,3,4,5-tetrakisphosphate on inositol 2,4,5-triphosphate-stimulated Ca2+ release do not involve direct interaction of inositol 1,3,4,5-tetrakisphosphate with inositol triphosphate-binding sites.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Defining signal transduction by inositol phosphates.Sub-cellular biochemistry · 2012Review
- Pharmacology of signaling induced by dopamine D(1)-like receptor activation.Pharmacology & therapeutics · 2010Review
- The regulation and function of inositol 1,4,5-trisphosphate 3-kinases.Advances in enzyme regulation · 2006Article
- Mechanisms of cross-talk between G-protein-coupled receptors resulting in enhanced release of intracellular Ca2+.The Biochemical journal · 2003Review
- Kinetic model of the inositol trisphosphate receptor that shows both steady-state and quantal patterns of Ca2+ release from intracellular stores.The Biochemical journal · 2003Article
- Molecular modelling and site-directed mutagenesis of the inositol 1,3,4,5-tetrakisphosphate-binding pleckstrin homology domain from the Ras GTPase-activating protein GAP1IP4BP.The Biochemical journal · 2000Article
- The effect of inositol 1,3,4,5-tetrakisphosphate on inositol trisphosphate-induced Ca2+ mobilization in freshly isolated and cultured mouse lacrimal acinar cells.The Biochemical journal · 2000Article
- Dual regulation of calcium mobilization by inositol 1,4, 5-trisphosphate in a living cell.The Journal of general physiology · 2000Article
- Protein-protein interactions in intracellular Ca2+-release channel function.The Biochemical journal · 1999Review
- Kinetics of elementary Ca2+ puffs evoked in Xenopus oocytes by different Ins(1,4,5)P3 receptor agonists.The Biochemical journal · 1998Article
- Modulation of Ins(2,4,5)P3-stimulated Ca2+ mobilization by ins(1,3,4, 5)P4: enhancement by activated G-proteins, and evidence for the involvement of a GAP1 protein, a putative Ins(1,3,4,5)P4 receptor.The Biochemical journal · 1998Article
- Metabolic evidence for PtdIns(4,5)P2-directed phospholipase C in permeabilized plant protoplasts.The Biochemical journal · 1997Article
- D-myo-inositol 1,4,5-trisphosphate 3-kinase A is activated by receptor activation through a calcium:calmodulin-dependent protein kinase II phosphorylation mechanism.The EMBO journal · 1997Article
- Rapid kinetic measurements of 45Ca2+ mobilization reveal that Ins(2,4,5)P3 is a partial agonist at hepatic InsP3 receptors.The Biochemical journal · 1997Article
- Ins(1,3,4,5)P4 is effective in mobilizing Ca2+ in mouse exocrine pancreatic acinar cells if phospholipase A2 is inhibited.The Biochemical journal · 1996Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We have previously found that for permeabilized L1210 cells, low micromolar concentrations of Ins(1,3,4,5)P4 added prior to Ins(2,4,5)P3 enhance the effects of suboptimal concentrations of Ins(2,4,5)P3 in causing Ca2+ release from InsP3-sensitive Ca2+ stores [Cullen, Irvine and Dawson (1990) Biochem J. 271, 549-553]. If this was due either to some conversion of added Ins(1,3,4,5)P4 into Ins(1,4,5)P3 by the 3-phosphatase, or to Ins(1,3,4,5)P4 acting as a weak (or partial) agonist on the InsP3 receptor it would be expected that,in the presence of thimerosal to sensitize the InsP3 receptor, the dose-response curve to Ins(1,3,4,5)P4 would be left-shifted by the same extent as that of Ins(1,4,5)P3. This was found not to be the case; the dose-response curve to Ins(1,3,4,5)P4 was not shifted at all by thimerosal. Furthermore, L-Ins(1,3,4,5)P4, which can displace radiolabelled D-Ins(1,3,4,5)P4 but not D-Ins(1,4,5)P3 from their respective high-affinity binding sites, mimicked the effects of D-Ins(1,3,4,5)P4 in enhancing the slow phase of Ins(2,4,5)P3-stimulated Ca2+ release. Ins(1,3,4,5)P4 caused an increase in magnitude of the slow phase of InsP3-stimulated Ca2+ release leaving the magnitude of the fast phase unaltered, in contrast to increasing Ins(2,4,5)P3 concentrations which increased the size of both phases. In addition, Ins(1,3,4,5)P4 decreased the rate constant for the slow phase of Ca2+ release. These findings point strongly to the conclusion that InsP4 is not working directly via the InsP3 receptor but indirectly via an InsP4 receptor.
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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.