File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Regulation of nuclear Ca2+ signaling by translocation of the Ca2+ messenger synthesizing enzyme ADP-ribosyl cyclase during neuronal depolarization

TitleRegulation of nuclear Ca2+ signaling by translocation of the Ca2+ messenger synthesizing enzyme ADP-ribosyl cyclase during neuronal depolarization
Authors
Issue Date2008
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, 2008, v. 283 n. 41, p. 27859-27870 How to Cite?
AbstractIn neurons, voltage-gated Ca2+ channels and nuclear Ca 2+ signaling play important roles, such as in the regulation of gene expression. However, the link between electrical activity and biochemical cascade activation involved in the generation of the nuclear Ca2+ signaling is poorly understood. Here we show that depolarization of Aplysia neurons induces the translocation of ADP-ribosyl cyclase, a Ca2+ messenger synthesizing enzyme, from the cytosol into the nucleus. The translocation is dependent on Ca2+ influx mainly through the voltage-dependent L-type Ca2+ channels. We report also that specific nucleoplasmic Ca2+ signals can be induced by three different calcium messengers, cyclic ADP-ribose, nicotinic acid adenine dinucleotide phosphate (NAADP), both produced by the ADP-ribosyl cyclase, and inositol 1,4,5-trisphosphate (IP3). Moreover, our pharmacological data show that NAADP acts on its own receptor, which cooperates with the IP3 and the ryanodine receptors to generate nucleoplasmic Ca2+ oscillations. We propose a new model where voltage-dependent L-type Ca 2+ channel-induced nuclear translocation of the cytosolic cyclase is a crucial step in the fine tuning of nuclear Ca2+ signals in neurons. © 2008 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/59678
ISSN
2020 Impact Factor: 5.157
2023 SCImago Journal Rankings: 1.766
ISI Accession Number ID
Funding AgencyGrant Number
Association Francaise contre les Myopathies and the Association pour la Recherche sur le Cancer
Funding Information:

The work was supported by grants from the Association Francaise contre les Myopathies and the Association pour la Recherche sur le Cancer (to J.-M. C.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

References

 

DC FieldValueLanguage
dc.contributor.authorBezin, Sen_HK
dc.contributor.authorCharpentier, Gen_HK
dc.contributor.authorLee, HCen_HK
dc.contributor.authorBaux, Gen_HK
dc.contributor.authorFossier, Pen_HK
dc.contributor.authorCancela, JMen_HK
dc.date.accessioned2010-05-31T03:55:05Z-
dc.date.available2010-05-31T03:55:05Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2008, v. 283 n. 41, p. 27859-27870en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59678-
dc.description.abstractIn neurons, voltage-gated Ca2+ channels and nuclear Ca 2+ signaling play important roles, such as in the regulation of gene expression. However, the link between electrical activity and biochemical cascade activation involved in the generation of the nuclear Ca2+ signaling is poorly understood. Here we show that depolarization of Aplysia neurons induces the translocation of ADP-ribosyl cyclase, a Ca2+ messenger synthesizing enzyme, from the cytosol into the nucleus. The translocation is dependent on Ca2+ influx mainly through the voltage-dependent L-type Ca2+ channels. We report also that specific nucleoplasmic Ca2+ signals can be induced by three different calcium messengers, cyclic ADP-ribose, nicotinic acid adenine dinucleotide phosphate (NAADP), both produced by the ADP-ribosyl cyclase, and inositol 1,4,5-trisphosphate (IP3). Moreover, our pharmacological data show that NAADP acts on its own receptor, which cooperates with the IP3 and the ryanodine receptors to generate nucleoplasmic Ca2+ oscillations. We propose a new model where voltage-dependent L-type Ca 2+ channel-induced nuclear translocation of the cytosolic cyclase is a crucial step in the fine tuning of nuclear Ca2+ signals in neurons. © 2008 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry . Copyright © American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.titleRegulation of nuclear Ca2+ signaling by translocation of the Ca2+ messenger synthesizing enzyme ADP-ribosyl cyclase during neuronal depolarizationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=283&spage=27859&epage= 27870&date=2008&atitle=Regulation+of+nuclear+Ca2++signalling+by+translocation+of+the+Ca2++messenger+synthesizing+enzyme+ADP-ribosyl+cyclase+during+neuronal+depolarization.en_HK
dc.identifier.emailLee, HC: leehc@hku.hken_HK
dc.identifier.authorityLee, HC=rp00545en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1074/jbc.M804701200en_HK
dc.identifier.pmid18632662en_HK
dc.identifier.scopuseid_2-s2.0-55549097127en_HK
dc.identifier.hkuros154341en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-55549097127&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume283en_HK
dc.identifier.issue41en_HK
dc.identifier.spage27859en_HK
dc.identifier.epage27870en_HK
dc.identifier.isiWOS:000259719200057-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridBezin, S=12785204800en_HK
dc.identifier.scopusauthoridCharpentier, G=7006583586en_HK
dc.identifier.scopusauthoridLee, HC=26642959100en_HK
dc.identifier.scopusauthoridBaux, G=7003436071en_HK
dc.identifier.scopusauthoridFossier, P=7003761734en_HK
dc.identifier.scopusauthoridCancela, JM=6701539634en_HK
dc.identifier.issnl0021-9258-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats