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Down-regulation of the neurotrophin receptor TrkB following ligand binding : evidence for an involvement of the proteasome and differential regulation of TrkA and TrkB

Sommerfeld, M. T. and Schweigreiter, R. and Barde, Y. A. and Hoppe, E.. (2000) Down-regulation of the neurotrophin receptor TrkB following ligand binding : evidence for an involvement of the proteasome and differential regulation of TrkA and TrkB. Journal of biological chemistry, Vol. 275 , no. 12. pp. 8982-8990.

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Official URL: http://edoc.unibas.ch/dok/A5259520

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Abstract

This study examines the mechanisms by which the tyrosine kinase receptor TrkB is down-regulated following binding of brain-derived neurotrophic factor (BDNF). In primary cultures of cerebellar granule neurons, BDNF-induced reduction of TrkB receptors was largely prevented by the addition of specific proteasome inhibitors. HN10 cells, a neuronal cell line that can be readily transfected, also showed a marked down-regulation of cell surface TrkB following BDNF exposure. In addition, we observed that prolonged exposure to nerve growth factor of TrkA-transfected cells did not lead to the down-regulation seen with BDNF and TrkB. TrkA and TrkB chimeric molecules were therefore expressed in HN10 cells and tested for ligand-induced regulation. These experiments led to the conclusion that the motives responsible for down-regulation are contained in the cytoplasmic domain of TrkB, and a short sequence in the juxtamembrane domain of TrkB was identified that confers nerve growth factor-induced down-regulation when inserted into TrkA.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Former Organization Units Biozentrum > Pharmacology/Neurobiology (Barde)
UniBasel Contributors:Barde, Yves-Alain
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:American Society of Biological Chemists
ISSN:0021-9258
Note:Publication type according to Uni Basel Research Database: Journal article
Last Modified:22 Mar 2012 14:21
Deposited On:22 Mar 2012 13:22

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