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Article: Structural determinants of Trk receptor specificities using BDNF-based neurotrophin chimeras

TitleStructural determinants of Trk receptor specificities using BDNF-based neurotrophin chimeras
Authors
Keywordsbrain-derived neurotrophic factor
chimeric neurotrophins
nerve growth factor
receptor tyrosine kinase
Issue Date1996
Citation
Journal of Neuroscience Research, 1996, v. 46 n. 5, p. 618-629 How to Cite?
AbstractNeurotrophins play very important roles in the development and maintenance of the vertebrate nervous system. In mammals, there are four members of the family: NGF, BDNF, NT-3, and NT-4/5. Members of the neurotrophin family activate different receptors that belong to a class of receptor tyrosine kinases known as 'Trks.' For example, NGF is the specific ligand of TrkA, while BDNF activates TrkB. To elucidate which regions of the two neurotrophins determine the receptor specificities, chimeric neurotrophins were constructed using BDNF as the backbone, with various regions being substituted by the corresponding regions of NGF. The activity of the chimeras on the Trk receptors was assayed in transfected fibroblasts ectopically expressing the Trk receptors. Our findings revealed that, although BDNF is absolutely conserved in mammals, substitution of several small variable regions from NGF into the BDNF backbone did not lead to significant loss in TrkB activity or gain in TrkA activity. Moreover, important determinants of TrkB activation might be located in the carboxy- terminal half of BDNF. On the other hand, critical elements for TrkA activation might be located within the amino-terminal half of the mature NGF molecule.
Persistent Identifierhttp://hdl.handle.net/10722/196617
ISSN
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 1.258
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, K-O-
dc.contributor.authorGlass, DJ-
dc.contributor.authorGeis, D-
dc.contributor.authorYancopoulos, GD-
dc.contributor.authorIp, NY-
dc.date.accessioned2014-04-24T02:10:28Z-
dc.date.available2014-04-24T02:10:28Z-
dc.date.issued1996-
dc.identifier.citationJournal of Neuroscience Research, 1996, v. 46 n. 5, p. 618-629-
dc.identifier.issn0360-4012-
dc.identifier.urihttp://hdl.handle.net/10722/196617-
dc.description.abstractNeurotrophins play very important roles in the development and maintenance of the vertebrate nervous system. In mammals, there are four members of the family: NGF, BDNF, NT-3, and NT-4/5. Members of the neurotrophin family activate different receptors that belong to a class of receptor tyrosine kinases known as 'Trks.' For example, NGF is the specific ligand of TrkA, while BDNF activates TrkB. To elucidate which regions of the two neurotrophins determine the receptor specificities, chimeric neurotrophins were constructed using BDNF as the backbone, with various regions being substituted by the corresponding regions of NGF. The activity of the chimeras on the Trk receptors was assayed in transfected fibroblasts ectopically expressing the Trk receptors. Our findings revealed that, although BDNF is absolutely conserved in mammals, substitution of several small variable regions from NGF into the BDNF backbone did not lead to significant loss in TrkB activity or gain in TrkA activity. Moreover, important determinants of TrkB activation might be located in the carboxy- terminal half of BDNF. On the other hand, critical elements for TrkA activation might be located within the amino-terminal half of the mature NGF molecule.-
dc.languageeng-
dc.relation.ispartofJournal of Neuroscience Research-
dc.subjectbrain-derived neurotrophic factor-
dc.subjectchimeric neurotrophins-
dc.subjectnerve growth factor-
dc.subjectreceptor tyrosine kinase-
dc.titleStructural determinants of Trk receptor specificities using BDNF-based neurotrophin chimeras-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/(SICI)1097-4547(19961201)46:5<618::AID-JNR10>3.0.CO;2-T-
dc.identifier.pmid8951673-
dc.identifier.scopuseid_2-s2.0-0029830402-
dc.identifier.volume46-
dc.identifier.issue5-
dc.identifier.spage618-
dc.identifier.epage629-
dc.identifier.isiWOS:A1996VW04400010-
dc.identifier.issnl0360-4012-

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