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Article: Nitric oxide-induced mobilization of intracellular calcium via the cyclic ADP-ribose signaling pathway

TitleNitric oxide-induced mobilization of intracellular calcium via the cyclic ADP-ribose signaling pathway
Authors
Issue Date1996
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 1996, v. 271 n. 7, p. 3699-3705 How to Cite?
AbstractCyclic adenosine diphosphate ribose (cADPR) is a potent endogenous calcium-mobilizing agent synthesized from β-NAD + by ADP-ribosyl cyclases in sea urchin eggs and in several mammalian cells (Galione, A., and White, A. (1994) Trends Cell Biol. 4, 431-436). Pharmacological studies suggest that cADPR is an endogenous modulator of Ca 2+-induced Ca 2+ release mediated by ryanodine-sensitive Ca 2+ release channels. An unresolved question is whether cADPR can act as a Ca 2+-mobilizing intracellular messenger. We show that exogenous application of nitric oxide (NO) mobilizes Ca 2+ from intracellular stores in intact sea urchin eggs and that it releases Ca 2+ and elevates cADPR levels in egg homogenates. 8-Amino-cADPR, a selective competitive antagonist of cADPR-mediated Ca 2+ release, and nicotinamide, an inhibitor of ADP-ribosyl cyclase, inhibit the Ca 2+-mobilizing actions of NO, while, heparin, a competitive antagonist of the inositol 1,4,5- trisphosphate receptor, did not affect NO-induced Ca 2+ release. Since the Ca 2+-mobilizing effects of NO can be mimicked by cGMP, are inhibited by the cGMP-dependent-protein kinase inhibitor, R(p)-8-pCPT-cGMPS, and in egg homogenates show a requirement for the guanylyl cyclase substrate, GTP, we suggest a novel action of NO in mobilizing intracellular calcium from microsomal stores via a signaling pathway involving cGMP and cADPR. These results suggest that cADPR has the capacity to act as a Ca 2+-mobilizing intracellular messenger.
Persistent Identifierhttp://hdl.handle.net/10722/171630
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
References

 

DC FieldValueLanguage
dc.contributor.authorWillmott, Nen_US
dc.contributor.authorSethi, JKen_US
dc.contributor.authorWalseth, TPen_US
dc.contributor.authorLee, HCen_US
dc.contributor.authorWhite, AMen_US
dc.contributor.authorGalione, Aen_US
dc.date.accessioned2012-10-30T06:16:03Z-
dc.date.available2012-10-30T06:16:03Z-
dc.date.issued1996en_US
dc.identifier.citationJournal Of Biological Chemistry, 1996, v. 271 n. 7, p. 3699-3705en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/171630-
dc.description.abstractCyclic adenosine diphosphate ribose (cADPR) is a potent endogenous calcium-mobilizing agent synthesized from β-NAD + by ADP-ribosyl cyclases in sea urchin eggs and in several mammalian cells (Galione, A., and White, A. (1994) Trends Cell Biol. 4, 431-436). Pharmacological studies suggest that cADPR is an endogenous modulator of Ca 2+-induced Ca 2+ release mediated by ryanodine-sensitive Ca 2+ release channels. An unresolved question is whether cADPR can act as a Ca 2+-mobilizing intracellular messenger. We show that exogenous application of nitric oxide (NO) mobilizes Ca 2+ from intracellular stores in intact sea urchin eggs and that it releases Ca 2+ and elevates cADPR levels in egg homogenates. 8-Amino-cADPR, a selective competitive antagonist of cADPR-mediated Ca 2+ release, and nicotinamide, an inhibitor of ADP-ribosyl cyclase, inhibit the Ca 2+-mobilizing actions of NO, while, heparin, a competitive antagonist of the inositol 1,4,5- trisphosphate receptor, did not affect NO-induced Ca 2+ release. Since the Ca 2+-mobilizing effects of NO can be mimicked by cGMP, are inhibited by the cGMP-dependent-protein kinase inhibitor, R(p)-8-pCPT-cGMPS, and in egg homogenates show a requirement for the guanylyl cyclase substrate, GTP, we suggest a novel action of NO in mobilizing intracellular calcium from microsomal stores via a signaling pathway involving cGMP and cADPR. These results suggest that cADPR has the capacity to act as a Ca 2+-mobilizing intracellular messenger.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.subject.meshAdp-Ribosyl Cyclaseen_US
dc.subject.meshAdenosine Diphosphate Ribose - Analogs & Derivatives - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cden_US
dc.subject.meshAntigens, Cd38en_US
dc.subject.meshAntigens, Differentiation - Metabolismen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCyclic Adp-Riboseen_US
dc.subject.meshCyclic Gmp - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGuanosine Triphosphate - Pharmacologyen_US
dc.subject.meshIsomerismen_US
dc.subject.meshKineticsen_US
dc.subject.meshMammalsen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshN-Glycosyl Hydrolases - Metabolismen_US
dc.subject.meshNad - Pharmacologyen_US
dc.subject.meshNiacinamide - Pharmacologyen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshOvum - Drug Effects - Physiologyen_US
dc.subject.meshSea Urchinsen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshThionucleotides - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.titleNitric oxide-induced mobilization of intracellular calcium via the cyclic ADP-ribose signaling pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLee, HC:leehc@hku.hken_US
dc.identifier.authorityLee, HC=rp00545en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.271.7.3699en_US
dc.identifier.pmid8631983-
dc.identifier.scopuseid_2-s2.0-0030044293en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030044293&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume271en_US
dc.identifier.issue7en_US
dc.identifier.spage3699en_US
dc.identifier.epage3705en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWillmott, N=7005919986en_US
dc.identifier.scopusauthoridSethi, JK=7006066648en_US
dc.identifier.scopusauthoridWalseth, TP=7005424273en_US
dc.identifier.scopusauthoridLee, HC=26642959100en_US
dc.identifier.scopusauthoridWhite, AM=24297306100en_US
dc.identifier.scopusauthoridGalione, A=7006334937en_US

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