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Journal ArticleDOI

Cyclic ADP-ribose in insulin secretion from pancreatic beta cells

Shin Takasawa, +3 more
- 15 Jan 1993 - 
- Vol. 259, Iss: 5093, pp 370-373
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TLDR
Results suggest that cADP-ribose is a mediator of calcium release from islet microsomes and may be generated in islets by glucose stimulation, serving as a second messenger for calcium mobilization in the endoplasmic reticulum.
Abstract
Inositol 1,4,5-trisphosphate (IP3) is thought to be a second messenger for intracellular calcium mobilization. However, in a cell-free system of islet microsomes, cyclic adenosine diphosphate-ribose (cADP-ribose), a nicotinamide adenine dinucleotide (NAD+) metabolite, but not IP3, induced calcium release. In digitonin-permeabilized islets, cADP-ribose and calcium, but not IP3, induced insulin secretion. Islet microsomes released calcium when combined with the extract from intact islets that had been incubated with high concentrations of glucose. Sequential additions of cADP-ribose inhibited the calcium release response to extracts from islets treated with high concentrations of glucose. Conversely, repeated additions of the islet extract inhibited the calcium release response to a subsequent addition of cADP-ribose. These results suggest that cADP-ribose is a mediator of calcium release from islet microsomes and may be generated in islets by glucose stimulation, serving as a second messenger for calcium mobilization in the endoplasmic reticulum.

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Citations
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Evolution and Function of the ADP Ribosyl Cyclase/CD38 Gene Family in Physiology and Pathology

TL;DR: CD38 is a powerful disease marker for human leukemias and myelomas, is directly involved in the pathogenesis and outcome of human immunodeficiency virus infection and chronic lymphocytic leukemia, and controls insulin release and the development of diabetes.
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Tyrosine kinases Lyn and Syk regulate B cell receptor-coupled Ca2+ mobilization through distinct pathways.

TL;DR: It is demonstrated that Syk mediates IP3 generation, whereas Lyn regulates Ca2+ mobilization through a process independent of IP3generation, despite the normal kinetics ofIP3 turnover.
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The ryanodine receptor/calcium channel genes are widely and differentially expressed in murine brain and peripheral tissues.

TL;DR: It is reported that the three ryanodine receptor genes are expressed in almost all tissues analyzed, which suggests that RyRs may participate in the regulation of intracellular calcium homeostasis in a range of cells wider than previously recognized.
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PKA-Dependent and PKA-Independent Pathways for cAMP-Regulated Exocytosis

TL;DR: Newly discovered cAMP-GEF/Epac mediates the PKA-independent effects on camp-regulated exocytosis, and localization of cAMP within intracellular compartments (cAMP compartmentation or compartmentalization) may be a key mechanism underlying the distinct effects of camp in different domains of the cell.
References
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Journal ArticleDOI

Inositol trisphosphate, a novel second messenger in cellular signal transduction.

TL;DR: Diacylglycerol operates within the plane of the membrane to activate protein kinase C, whereas inositol trisphosphate is released into the cytoplasm to function as a second messenger for mobilizing intracellular calcium.
Journal ArticleDOI

Photochemically generated cytosolic calcium pulses and their detection by fluo-3.

TL;DR: It is demonstrated that fluo-3 can be loaded into fibroblasts and lymphocytes by incubation with the pentaacetoxymethyl ester of the dye and that the ester is hydrolyzed intracellularly to yield genuine flui-3 capable of indicating changes in [Ca2+]i induced by agonist stimulation.
Journal ArticleDOI

Ca(2+)-induced Ca2+ release in sea urchin egg homogenates: modulation by cyclic ADP-ribose.

TL;DR: Cyclic ADP-ribose, a metabolite with potent Ca(2+)-releasing properties, appears to act by way of the CICR mechanism and may thus be an endogenous modulator of C ICR.
Journal ArticleDOI

Streptozotocin and alloxan induce DNA strand breaks and poly(ADP-ribose) synthetase in pancreatic islets.

TL;DR: It is described that both Streptozotocin and alloxan cause DNA strand breaks which stimulate nuclear poly(ADP–ribose) synthetase, thereby depleting intracellular NAD and inhibiting proinsulin synthesis in isolated pancreatic islets of rats.
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