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- Publisher Website: 10.1074/jbc.M601863200
- Scopus: eid_2-s2.0-33744925451
- PMID: 16611639
- WOS: WOS:000237996000007
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Article: STAT3 as a downstream mediator of Trk signaling and functions
Title | STAT3 as a downstream mediator of Trk signaling and functions |
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Authors | |
Keywords | Chemicals 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 Date | 2006 |
Publisher | American 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? |
Abstract | Signal 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 Identifier | http://hdl.handle.net/10722/145823 |
ISSN | 2020 Impact Factor: 5.157 2023 SCImago Journal Rankings: 1.766 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yu, PN | en_HK |
dc.contributor.author | Cheung, ZH | en_HK |
dc.contributor.author | Ip, NY | en_HK |
dc.date.accessioned | 2012-03-23T09:49:50Z | - |
dc.date.available | 2012-03-23T09:49:50Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | Journal Of Biological Chemistry, 2006, v. 281 n. 23, p. 15636-15644 | en_HK |
dc.identifier.issn | 0021-9258 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/145823 | - |
dc.description.abstract | Signal 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.language | eng | en_US |
dc.publisher | American Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/ | en_HK |
dc.relation.ispartof | Journal of Biological Chemistry | en_HK |
dc.subject | Chemicals And Cas Registry Numbers: Nerve Growth Factor, 9061-61-4 | en_US |
dc.subject | Brain-Derived Neurotrophic Factor | en_US |
dc.subject | Dna Primers | en_US |
dc.subject | Nerve Growth Factor, 9061-61-4 | en_US |
dc.subject | Receptor, Trka, Ec 2.7.1.112 | en_US |
dc.subject | Stat3 Transcription Factor | en_US |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Base Sequence | en_HK |
dc.subject.mesh | Brain-Derived Neurotrophic Factor - pharmacology | en_HK |
dc.subject.mesh | Cells, Cultured | en_HK |
dc.subject.mesh | DNA Primers | en_HK |
dc.subject.mesh | Hippocampus - cytology - drug effects - metabolism | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | Nerve Growth Factor - pharmacology | en_HK |
dc.subject.mesh | Neurons - drug effects - metabolism | en_HK |
dc.subject.mesh | PC12 Cells | en_HK |
dc.subject.mesh | Phosphorylation | en_HK |
dc.subject.mesh | Rats | en_HK |
dc.subject.mesh | Receptor, trkA - metabolism | en_HK |
dc.subject.mesh | STAT3 Transcription Factor - metabolism - physiology | en_HK |
dc.subject.mesh | Signal Transduction - physiology | en_HK |
dc.subject.mesh | Subcellular Fractions - metabolism | en_HK |
dc.subject.mesh | Transcription, Genetic - physiology | en_HK |
dc.title | STAT3 as a downstream mediator of Trk signaling and functions | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Cheung, ZH:zelda@hku.hk | en_HK |
dc.identifier.authority | Cheung, ZH=rp01588 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1074/jbc.M601863200 | en_HK |
dc.identifier.pmid | 16611639 | - |
dc.identifier.scopus | eid_2-s2.0-33744925451 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33744925451&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 281 | en_HK |
dc.identifier.issue | 23 | en_HK |
dc.identifier.spage | 15636 | en_HK |
dc.identifier.epage | 15644 | en_HK |
dc.identifier.eissn | 1083-351X | - |
dc.identifier.isi | WOS:000237996000007 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Yu, PN=14008420100 | en_HK |
dc.identifier.scopusauthorid | Cheung, ZH=6507483375 | en_HK |
dc.identifier.scopusauthorid | Ip, NY=7005756760 | en_HK |
dc.identifier.issnl | 0021-9258 | - |