Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate

  title={Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate},
  author={Holger Streb and Robin F. Irvine and Michael John Berridge and Irene Schulz},
Activation of receptors for a wide variety of hormones and neurotransmitters leads to an increase in the intracellular level of calcium. Much of this calcium is released from intracellular stores but the link between surface receptors and this internal calcium reservoir is unknown. Hydrolysis of the phosphoinositides, which is another characteristic feature of these receptors1–3, has been implicated in calcium mobilization1. The primary lipid substrates for the receptor mechanism seem to be two… Expand
Rapid mobilization of Ca2+ from rat insulinoma microsomes by inositol-1,4,5-trisphosphate
It is shown directly that Ins1,4,5P3 rapidly releases Ca2+ from a microsomal fraction of rat insulinoma but not from mitochondria or secretory granules, suggesting that Ins2+ mobilization from internal pools is not mediated. Expand
Inositol phosphate metabolism and signal transduction.
A recent proposal that (1,4,5)IP3, by emptying an intracellular Ca2+ pool, secondarily elicits Ca2- entry will be considered. Expand
Ion channels activated by inositol 1,4,5-trisphosphate in plasma membrane of human T-lymphocytes
It is suggested that Ins(1,4,5)P3 acts as the second messenger mediating transmembrane Ca2+ influx through specific Ca2-permeable channels in mitogen-stimulated T-cell activation. Expand
The Ins(1,4,5)P3-sensitive Ca2+ store of non-muscle cells: endoplasmic reticulum or calciosomes?
It is demonstrated that there is no correlation between the abundance of ER and the amount Ins(1,4,5)P3-sensitive Ca2+ release and evidence is provided for the existence of an unrecognized organelle, the 'calciosome', which appears to be morphologically distinct from any other known cell organelle. Expand
Specific Receptors for Inositol 1,4,5-Trisphosphate in Endocrine Target Tissues
The hydrolysis of inositol lipids by phospholipase C is believed to be the primary mechanism by which many hormones elicit calcium-mediated metabolic and secretory responses in their respectiveExpand
The phosphoinositide signalling system. I. Historical background. II. Effects of lithium on the accumulation of second messenger inositol 1,4,5-trisphosphate in brain cortex slices.
Inositol lipids in cell membranes are cleaved to inositol phosphates and diacylglycerol, which activates protein kinase C, which phosphorylates a different set of proteins, leading to a variety of biological responses. Expand
Inositol phosphate formation and its relationship to calcium signaling.
Current understanding of the mechanisms by which inositol phosphates regulate cytoplasmic Ca2+ concentrations is summarized. Expand
Activation of the Inositol-1,4,5-Trisphosphate Signaling System by Acute Ethanol Treatment of Rat Hepatocytes
A large number of hormones and other agonists bring about their intracellular effects through an elevation of cytosolic free Ca2+ concentration. The mechanism by which this elevation of cytosolicExpand
Inositol 1,4,5-trisphosphate releases Ca2+ from a nonmitochondrial store site in permeabilized rat cortical kidney cells.
Investigation of the effect of angiotensin II-amide and IP3 on intracellular Ca2 stores in saponin-treated cells and homogenate from rat kidney cortex suggests that IP3, one of their hydrolysis products, increases during hormonal stimulation. Expand
Modulation of inositol(1,4,5)trisphosphate-sensitive calcium store content during continuous receptor activation and its effects on calcium entry.
Changes in intracellular Ca2+ concentration following the activation of muscarinic receptors with carbachol were studied in cells from the exocrine avian nasal gland and it was concluded that the subsequent effect of thapsigargin was due to a partial refilling of the Ins(1,4,5)P3-sensitive stores despite the continued presence of agonist. Expand


Receptor-mediated net breakdown of phosphatidylinositol 4,5-bisphosphate in parotid acinar cells.
Results may suggest that net PtdIns(4,5)P2 breakdown is an early event in the stimulus-response pathway of the parotid acinar cell and could be directly involved in the mechanism of agonist-induced Ca2+ release from the plasma membrane. Expand
Changes in the levels of inositol phosphates after agonist-dependent hydrolysis of membrane phosphoinositides.
The results suggest that the earliest event in the stimulus-response pathway is the hydrolysis of polyphosphoinositides by a phosphodiesterase to yield inositol 1,4,5-trisphosphate and inositl 1, 4-bisph phosphate, which are subsequently hydrolysed to inositoli 1-phosphates and inposol. Expand
Rapid accumulation of inositol trisphosphate reveals that agonists hydrolyse polyphosphoinositides instead of phosphatidylinositol.
  • M. Berridge
  • Biology, Medicine
  • The Biochemical journal
  • 1983
The primary action of 5-hydroxytryptamine is to stimulate the hydrolysis of PtdIns(4,5)P2 to yield diacylglycerol and Ins(1,4,4)P3, which suggests that they could function as second messengers, perhaps to control the release of calcium from internal pools. Expand
Hormone-stimulated metabolism of inositol lipids and its relationship to hepatic receptor function.
It seems that vasopressin-stimulated PtdIns degradation in hepatocytes is not a consequence of intracellular Ca2+-mobilization and it appears instead to be intimately coupled to receptor occupation. Expand
Rapid decrease of phosphatidylinositol 4,5-bisphosphate in thrombin-stimulated platelets.
It appears that thrombin causes a rapid and transient degradation of phosphatidylinositol 4,5-bisphosphate and that this effect might be related to the initiation of platelet activation. Expand
Effects of secretagogues on [32P]phosphatidylinositol 4,5-bisphosphate metabolism in the exocrine pancreas.
The results suggest that agonist-induced PtdIns(4,5)P2 breakdown in the exocrine pancreas may be an early step in the stimulus-response coupling pathway and also suggest that this breakdown is not dependent on Ca2+-mobilization. Expand
The inositol trisphosphate phosphomonoesterase of the human erythrocyte membrane.
It is suggested that this enzyme is selective for the 5-phosphate in those water-soluble phosphate esters of inositol that possess the vicinal pair of 4,5-ph phosphates but that it may also interact less strongly with other water- soluble compounds that have pairs of vicinal phosphates. Expand
Compartmentation of calcium in digitonin-disrupted guinea pig pancreatic acinar cells.
The treatment of guinea pig pancreatic acinar cells with digitonin leads to disruption of the plasma membrane, as judged by the liberation of cytosolic enzymes, without significant alteration of theExpand
Thrombin-induced phosphodiesteratic cleavage of phosphatidylinositol bisphosphate in human platelets.
The addition of thrombin to human platelets prelabeled with 32Pi led to significant loss of radioactivity in phosphatidylinositol 4,5-bisphosphate within 5 s, followed by recovery or even increase by 2 min, which suggests that a pool of polyphosphoinositides is constantly undergoing phosphodiesteratic cleavage and resynthesis. Expand
The hydrolysis of phosphatidylinositol by lysosomal enzymes of rat liver and brain.
Evidence is presented that an EDTA-insensitive phospholipase C degrading phosphatidylinositol is present in rat brain. Expand