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Article: Endophilin B1 as a novel regulator of nerve growth factor/TrkA trafficking and neurite outgrowth

TitleEndophilin B1 as a novel regulator of nerve growth factor/TrkA trafficking and neurite outgrowth
Authors
KeywordsEndosomes
Neurite outgrowth
Neurotrophin
Receptor trafficking
Receptor tyrosine kinase
Trk receptors
Issue Date2008
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
Journal Of Neuroscience, 2008, v. 28 n. 36, p. 9002-9012 How to Cite?
AbstractNeurotrophins and their cognate receptors Trks are important regulators of neuronal survival and differentiation. Recent studies reveal that internalization and trafficking of Trks play a critical role in neurotrophin-mediated signaling. At present, little is known of the molecular events that mediate this process. In the current study, we show that endophilin B1 is a novel regulator of nerve growth factor (NGF) trafficking.Wefound that endophilin B1 interacts with both TrkA and early endosome marker EEA1. Interestingly, knockdown of endophilin B1 results in enlarged EEA1-positive vesicles in NGF-treated PC12 cells. This is accompanied by increased lysosomal targeting of NGF/TrkA and TrkA degradation, and reduced total TrkA levels. In addition, knockdown of endophilin B1 attenuates Erk1/2 activation in the endosomal fraction after NGF treatment. This is accompanied by a marked inhibition of NGF-induced gene transcription and neurite outgrowth in endophilin B1-knocked down cells. Our observations implicate endophilin B1 as a novel regulator of NGF trafficking, thereby affecting TrkA levels and downstream signaling on endosomes to mediate biological functions of NGF. Copyright © 2008 Society for Neuroscience.
Persistent Identifierhttp://hdl.handle.net/10722/145815
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKUST 6119/04M
6431/06M
661007
HKUST 3/03C
Area of Excellence Scheme of the University Grants CommitteeAoE/B-15/01
Funding Information:

This work was supported in part by the Research Grants Council of Hong Kong (HKUST 6119/04M, 6431/06M, 661007, and HKUST 3/03C) and the Area of Excellence Scheme of the University Grants Committee (AoE/B-15/01). N.Y.I. and Z.H.C. are Croucher Foundation Senior Research Fellow and Croucher Foundation Fellow, respectively. We thank Winnie Chien, Cong Yu, and Yihang Li for their excellent technical assistance. We are also grateful to Dr. Amy Fu for critical reading of this manuscript and to members of the Ip Laboratory for many helpful discussions.

References

 

DC FieldValueLanguage
dc.contributor.authorWan, Jen_HK
dc.contributor.authorCheung, AYen_HK
dc.contributor.authorFu, WYen_HK
dc.contributor.authorWu, Cen_HK
dc.contributor.authorZhang, Men_HK
dc.contributor.authorMobley, WCen_HK
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorIp, NYen_HK
dc.date.accessioned2012-03-23T09:49:46Z-
dc.date.available2012-03-23T09:49:46Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Neuroscience, 2008, v. 28 n. 36, p. 9002-9012en_HK
dc.identifier.issn0270-6474en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145815-
dc.description.abstractNeurotrophins and their cognate receptors Trks are important regulators of neuronal survival and differentiation. Recent studies reveal that internalization and trafficking of Trks play a critical role in neurotrophin-mediated signaling. At present, little is known of the molecular events that mediate this process. In the current study, we show that endophilin B1 is a novel regulator of nerve growth factor (NGF) trafficking.Wefound that endophilin B1 interacts with both TrkA and early endosome marker EEA1. Interestingly, knockdown of endophilin B1 results in enlarged EEA1-positive vesicles in NGF-treated PC12 cells. This is accompanied by increased lysosomal targeting of NGF/TrkA and TrkA degradation, and reduced total TrkA levels. In addition, knockdown of endophilin B1 attenuates Erk1/2 activation in the endosomal fraction after NGF treatment. This is accompanied by a marked inhibition of NGF-induced gene transcription and neurite outgrowth in endophilin B1-knocked down cells. Our observations implicate endophilin B1 as a novel regulator of NGF trafficking, thereby affecting TrkA levels and downstream signaling on endosomes to mediate biological functions of NGF. Copyright © 2008 Society for Neuroscience.en_HK
dc.languageengen_US
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.orgen_HK
dc.relation.ispartofJournal of Neuroscienceen_HK
dc.subjectEndosomesen_HK
dc.subjectNeurite outgrowthen_HK
dc.subjectNeurotrophinen_HK
dc.subjectReceptor traffickingen_HK
dc.subjectReceptor tyrosine kinaseen_HK
dc.subjectTrk receptorsen_HK
dc.titleEndophilin B1 as a novel regulator of nerve growth factor/TrkA trafficking and neurite outgrowthen_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.doi10.1523/JNEUROSCI.0767-08.2008en_HK
dc.identifier.scopuseid_2-s2.0-54049139685en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54049139685&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue36en_HK
dc.identifier.spage9002en_HK
dc.identifier.epage9012en_HK
dc.identifier.eissn1529-2401-
dc.identifier.isiWOS:000258890900017-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWan, J=35320527600en_HK
dc.identifier.scopusauthoridCheung, AY=25421547900en_HK
dc.identifier.scopusauthoridFu, WY=7202947428en_HK
dc.identifier.scopusauthoridWu, C=7501665750en_HK
dc.identifier.scopusauthoridZhang, M=7601555100en_HK
dc.identifier.scopusauthoridMobley, WC=7006497542en_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridIp, NY=7005756760en_HK

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