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Article: Differential effects of glial cell line-derived neurotrophic factor and neurturin in RET/GFRα1-expressing cells

TitleDifferential effects of glial cell line-derived neurotrophic factor and neurturin in RET/GFRα1-expressing cells
Authors
KeywordsNeurite outgrowth
Neuron
Neurotrophic factors
Receptor tyrosine kinase
Survival
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828
Citation
Journal Of Neuroscience Research, 2006, v. 83 n. 1, p. 80-90 How to Cite?
AbstractThe c-ret protooncogene, RET, encodes a receptor tyrosine kinase. RET is activated by members of the glial cell line-derived neurotrophic factor (GDNF) family of ligands, which include GDNF, neurturin, artemin, and persephin. The ligands bind RET through GDNF family receptor α, termed GFRα1-4. Despite the importance of RET signaling in the development of the enteric nervous system and the kidney, the differential signaling mechanisms between RET ligands are poorly established. It has been suggested that signal specificity is achieved through binding of the ligand to its preferred GFRα. To compare the signaling profiles of GDNF and neurturin, we have identified a cell line, NG108-15, which endogenously expresses RET and GFRα1 but not GFRα2-4. Immunoblot data showed that GDNF caused a transient activation, whereas neurturin caused a sustained activation, of both p44/p42 MAP kinases and PLC-γ. Under serum starvation, NG108-15 cells differentiate and form neuntes. Neurturin but not GDNF stimulated neurite outgrowth, which could be blocked by the selective PLC inhibitor U73122. On the other hand, GDNF but not neurturin promoted cell survival, and this could be blocked by the p44/p42 MAP kinase inhibitor PD98059. Our findings not only show the differential signaling of GDNF and neurturin but also suggest that this can be achieved through binding to the same GFRα subtype, leading to distinct biological responses. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/170362
ISSN
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 1.258
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, RHKen_US
dc.contributor.authorWong, WLen_US
dc.contributor.authorChan, CHen_US
dc.contributor.authorChan, SYen_US
dc.date.accessioned2012-10-30T06:07:48Z-
dc.date.available2012-10-30T06:07:48Z-
dc.date.issued2006en_US
dc.identifier.citationJournal Of Neuroscience Research, 2006, v. 83 n. 1, p. 80-90en_US
dc.identifier.issn0360-4012en_US
dc.identifier.urihttp://hdl.handle.net/10722/170362-
dc.description.abstractThe c-ret protooncogene, RET, encodes a receptor tyrosine kinase. RET is activated by members of the glial cell line-derived neurotrophic factor (GDNF) family of ligands, which include GDNF, neurturin, artemin, and persephin. The ligands bind RET through GDNF family receptor α, termed GFRα1-4. Despite the importance of RET signaling in the development of the enteric nervous system and the kidney, the differential signaling mechanisms between RET ligands are poorly established. It has been suggested that signal specificity is achieved through binding of the ligand to its preferred GFRα. To compare the signaling profiles of GDNF and neurturin, we have identified a cell line, NG108-15, which endogenously expresses RET and GFRα1 but not GFRα2-4. Immunoblot data showed that GDNF caused a transient activation, whereas neurturin caused a sustained activation, of both p44/p42 MAP kinases and PLC-γ. Under serum starvation, NG108-15 cells differentiate and form neuntes. Neurturin but not GDNF stimulated neurite outgrowth, which could be blocked by the selective PLC inhibitor U73122. On the other hand, GDNF but not neurturin promoted cell survival, and this could be blocked by the p44/p42 MAP kinase inhibitor PD98059. Our findings not only show the differential signaling of GDNF and neurturin but also suggest that this can be achieved through binding to the same GFRα subtype, leading to distinct biological responses. © 2005 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828en_US
dc.relation.ispartofJournal of Neuroscience Researchen_US
dc.rightsJournal of Neuroscience Research. Copyright © John Wiley & Sons, Inc.-
dc.subjectNeurite outgrowth-
dc.subjectNeuron-
dc.subjectNeurotrophic factors-
dc.subjectReceptor tyrosine kinase-
dc.subjectSurvival-
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Neoplasms - Metabolism - Pathologyen_US
dc.subject.meshCell Differentiation - Genetics - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movement - Physiologyen_US
dc.subject.meshCell Survival - Genetics - Physiologyen_US
dc.subject.meshGlial Cell Line-Derived Neurotrophic Factor - Pharmacologyen_US
dc.subject.meshGlial Cell Line-Derived Neurotrophic Factor Receptors - Genetics - Physiologyen_US
dc.subject.meshImmunoblottingen_US
dc.subject.meshLigandsen_US
dc.subject.meshMitogen-Activated Protein Kinase 3 - Geneticsen_US
dc.subject.meshNeuroblastoma - Metabolism - Pathologyen_US
dc.subject.meshNeurons - Drug Effects - Physiologyen_US
dc.subject.meshNeurturin - Pharmacologyen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProto-Oncogene Proteins C-Ret - Genetics - Physiologyen_US
dc.subject.meshRna - Biosynthesis - Geneticsen_US
dc.subject.meshRatsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshTyrosine - Metabolismen_US
dc.titleDifferential effects of glial cell line-derived neurotrophic factor and neurturin in RET/GFRα1-expressing cellsen_US
dc.typeArticleen_US
dc.identifier.emailChan, SY:sychan@hkucc.hku.hken_US
dc.identifier.emailLee, RHK: jrebecca@hkusua.hku.hk-
dc.identifier.authorityChan, SY=rp00356en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jnr.20701en_US
dc.identifier.pmid16294336-
dc.identifier.scopuseid_2-s2.0-30344447532en_US
dc.identifier.hkuros115916-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-30344447532&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume83en_US
dc.identifier.issue1en_US
dc.identifier.spage80en_US
dc.identifier.epage90en_US
dc.identifier.eissn1097-4547-
dc.identifier.isiWOS:000234677600009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLee, RHK=11142046100en_US
dc.identifier.scopusauthoridWong, WL=25937066400en_US
dc.identifier.scopusauthoridChan, CH=7404814177en_US
dc.identifier.scopusauthoridChan, SY=7404255082en_US
dc.identifier.issnl0360-4012-

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