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Article: CD38/cADPR/Ca 2+ pathway promotes cell proliferation and delays nerve growth factor-induced differentiation in PC12 cells

TitleCD38/cADPR/Ca 2+ pathway promotes cell proliferation and delays nerve growth factor-induced differentiation in PC12 cells
Authors
Issue Date2009
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, 2009, v. 284 n. 43, p. 29335-29342 How to Cite?
AbstractIntracellular Ca 2+ mobilization plays an important role in a wide variety of cellular processes, and multiple second messengers are responsible for mediating intracellular Ca 2+ changes. Here we explored the role of one endogenous Ca 2+ -mobilizing nucleotide, cyclic adenosine diphosphoribose (cADPR), in the proliferation and differentiation of neurosecretory PC12 cells. We found that cADPR induced Ca 2+ release in PC12 cells and that CD38 is the main ADP-ribosyl cyclase responsible for the acetylcholine (ACh)-induced cADPR production in PC12 cells. In addition, the CD38/ cADPR signaling pathway is shown to be required for the ACh-induced Ca 2+ increase and cell proliferation. Inhibition of the pathway, on the other hand, accelerated nerve growth factor (NGF)-induced neuronal differentiation in PC12 cells. Conversely, overexpression of CD38 increased cell proliferation but delayed NGF-induced differentiation. Our data indicate that cADPR plays a dichotomic role in regulating proliferation and neuronal differentiation of PC12 cells. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/171779
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYue, Jen_US
dc.contributor.authorWei, Wen_US
dc.contributor.authorLam, CMCen_US
dc.contributor.authorZhao, YJen_US
dc.contributor.authorDong, Men_US
dc.contributor.authorZhang, LRen_US
dc.contributor.authorZhang, LHen_US
dc.contributor.authorLee, HCen_US
dc.date.accessioned2012-10-30T06:17:02Z-
dc.date.available2012-10-30T06:17:02Z-
dc.date.issued2009en_US
dc.identifier.citationJournal Of Biological Chemistry, 2009, v. 284 n. 43, p. 29335-29342en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/171779-
dc.description.abstractIntracellular Ca 2+ mobilization plays an important role in a wide variety of cellular processes, and multiple second messengers are responsible for mediating intracellular Ca 2+ changes. Here we explored the role of one endogenous Ca 2+ -mobilizing nucleotide, cyclic adenosine diphosphoribose (cADPR), in the proliferation and differentiation of neurosecretory PC12 cells. We found that cADPR induced Ca 2+ release in PC12 cells and that CD38 is the main ADP-ribosyl cyclase responsible for the acetylcholine (ACh)-induced cADPR production in PC12 cells. In addition, the CD38/ cADPR signaling pathway is shown to be required for the ACh-induced Ca 2+ increase and cell proliferation. Inhibition of the pathway, on the other hand, accelerated nerve growth factor (NGF)-induced neuronal differentiation in PC12 cells. Conversely, overexpression of CD38 increased cell proliferation but delayed NGF-induced differentiation. Our data indicate that cADPR plays a dichotomic role in regulating proliferation and neuronal differentiation of PC12 cells. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.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.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.-
dc.titleCD38/cADPR/Ca 2+ pathway promotes cell proliferation and delays nerve growth factor-induced differentiation in PC12 cellsen_US
dc.typeArticleen_US
dc.identifier.emailYue, J:jyue@hku.hken_US
dc.identifier.emailLee, HC:leehc@hku.hken_US
dc.identifier.emailWei, W: wenjiewei2007@gmail.com-
dc.identifier.emailLam, MC: boconnie@gmail.com-
dc.identifier.emailZhao, Y: zhaoyongjuan@gmail.com-
dc.identifier.authorityYue, J=rp00286en_US
dc.identifier.authorityLee, HC=rp00545en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1074/jbc.M109.049767en_US
dc.identifier.pmid19696022-
dc.identifier.pmcidPMC2785564-
dc.identifier.scopuseid_2-s2.0-70350350042en_US
dc.identifier.hkuros167821-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350350042&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume284en_US
dc.identifier.issue43en_US
dc.identifier.spage29335en_US
dc.identifier.epage29342en_US
dc.identifier.eissn1083-351X-
dc.identifier.isiWOS:000270896800013-
dc.publisher.placeUnited Statesen_US
dc.identifier.f10001163654-
dc.identifier.scopusauthoridYue, J=7101875828en_US
dc.identifier.scopusauthoridWei, W=35219493500en_US
dc.identifier.scopusauthoridLam, CMC=26026006700en_US
dc.identifier.scopusauthoridZhao, YJ=35219477000en_US
dc.identifier.scopusauthoridDong, M=36571659600en_US
dc.identifier.scopusauthoridZhang, LR=8833065300en_US
dc.identifier.scopusauthoridZhang, LH=10340097000en_US
dc.identifier.scopusauthoridLee, HC=26642959100en_US

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