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Article: STAT3 as a downstream mediator of Trk signaling and functions

TitleSTAT3 as a downstream mediator of Trk signaling and functions
Authors
KeywordsChemicals And Cas Registry Numbers: Nerve Growth Factor, 9061-61-4
Brain-Derived Neurotrophic Factor
Dna Primers
Nerve Growth Factor, 9061-61-4
Receptor, Trka, Ec 2.7.1.112
Stat3 Transcription Factor
Issue Date2006
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, 2006, v. 281 n. 23, p. 15636-15644 How to Cite?
AbstractSignal transducer and activator of transcription 3 (STAT3) has long been shown to regulate gene transcription in response to cytokines and growth factors. Recent evidence suggests that STAT3 activation may also occur downstream of receptor-tyrosine kinase activation. In the current study we have identified STAT3 as a novel signal transducer for TrkA, the receptor-tyrosine kinase that mediates the functions of nerve growth factor (NGF). Activation of TrkA by NGF triggered STAT3 phosphorylation at Ser-727, and enhanced the DNA binding and transcriptional activities of STAT3. More importantly, neurotrophin-induced increase in STAT3 activation was observed to underlie several downstream functions of neurotrophin signaling. First of all, knockdown of STAT3 expression using the RNA interference approach attenuated NGF-induced transcription of immediate early genes in PC12 cells. Furthermore, reduced STAT3 expression in PC12 cells suppressed NGF-induced cyclin D1 expression, thereby inhibiting growth arrest normally triggered by NGF treatment. Finally, inhibition of STAT3 expression decreased brain-derived neurotrophic factor-promoted neurite outgrowth in primary hippocampal neurons. Together, our findings have identified STAT3 as an essential component of neurotrophin signaling and functions. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/145823
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, PNen_HK
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorIp, NYen_HK
dc.date.accessioned2012-03-23T09:49:50Z-
dc.date.available2012-03-23T09:49:50Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2006, v. 281 n. 23, p. 15636-15644en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145823-
dc.description.abstractSignal transducer and activator of transcription 3 (STAT3) has long been shown to regulate gene transcription in response to cytokines and growth factors. Recent evidence suggests that STAT3 activation may also occur downstream of receptor-tyrosine kinase activation. In the current study we have identified STAT3 as a novel signal transducer for TrkA, the receptor-tyrosine kinase that mediates the functions of nerve growth factor (NGF). Activation of TrkA by NGF triggered STAT3 phosphorylation at Ser-727, and enhanced the DNA binding and transcriptional activities of STAT3. More importantly, neurotrophin-induced increase in STAT3 activation was observed to underlie several downstream functions of neurotrophin signaling. First of all, knockdown of STAT3 expression using the RNA interference approach attenuated NGF-induced transcription of immediate early genes in PC12 cells. Furthermore, reduced STAT3 expression in PC12 cells suppressed NGF-induced cyclin D1 expression, thereby inhibiting growth arrest normally triggered by NGF treatment. Finally, inhibition of STAT3 expression decreased brain-derived neurotrophic factor-promoted neurite outgrowth in primary hippocampal neurons. Together, our findings have identified STAT3 as an essential component of neurotrophin signaling and functions. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
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_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.subjectChemicals And Cas Registry Numbers: Nerve Growth Factor, 9061-61-4en_US
dc.subjectBrain-Derived Neurotrophic Factoren_US
dc.subjectDna Primersen_US
dc.subjectNerve Growth Factor, 9061-61-4en_US
dc.subjectReceptor, Trka, Ec 2.7.1.112en_US
dc.subjectStat3 Transcription Factoren_US
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBrain-Derived Neurotrophic Factor - pharmacologyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshHippocampus - cytology - drug effects - metabolismen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshNerve Growth Factor - pharmacologyen_HK
dc.subject.meshNeurons - drug effects - metabolismen_HK
dc.subject.meshPC12 Cellsen_HK
dc.subject.meshPhosphorylationen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReceptor, trkA - metabolismen_HK
dc.subject.meshSTAT3 Transcription Factor - metabolism - physiologyen_HK
dc.subject.meshSignal Transduction - physiologyen_HK
dc.subject.meshSubcellular Fractions - metabolismen_HK
dc.subject.meshTranscription, Genetic - physiologyen_HK
dc.titleSTAT3 as a downstream mediator of Trk signaling and functionsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M601863200en_HK
dc.identifier.pmid16611639-
dc.identifier.scopuseid_2-s2.0-33744925451en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33744925451&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume281en_HK
dc.identifier.issue23en_HK
dc.identifier.spage15636en_HK
dc.identifier.epage15644en_HK
dc.identifier.eissn1083-351X-
dc.identifier.isiWOS:000237996000007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYu, PN=14008420100en_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridIp, NY=7005756760en_HK

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