Glial cell line-derived neurotrophic factor signals through the RET receptor and activates mitogen-activated protein kinase

Carolyn A. Worby, Quinn Vega, Yi Zhao, Hanna H.J. Chao, Audrey F. Seasholtz, Jack E. Dixon

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Abstract

Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming growth factor-β family of growth factors, was first identified by its ability to promote the survival of midbrain dopaminergic neurons in culture. We demonstrate that GDNF treatment of several neuroblastoma cell lines leads to dose-dependent tyrosine phosphorylation of the RET receptor and that other transforming growth factor-β family members are not able to activate the RET receptor. GDNF treatment of neuroblastoma cells also results in increased transcription of an Elk luciferase reporter gene, suggesting that GDNF activates the mitogen-activated protein kinase signal transduction pathway.

Original languageEnglish
Pages (from-to)23619-23622
Number of pages4
JournalJournal of Biological Chemistry
Volume271
Issue number39
DOIs
StatePublished - 10 Oct 1996

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Glial Cell Line-Derived Neurotrophic Factor
Mitogen-Activated Protein Kinases
Transforming Growth Factors
Neuroblastoma
Signal transduction
Phosphorylation
Aptitude
Dopaminergic Neurons
Transcription
Mesencephalon
Luciferases
Reporter Genes
Neurons
Tyrosine
Signal Transduction
Intercellular Signaling Peptides and Proteins
Genes
Cells
Cell Line

Cite this

Worby, Carolyn A. ; Vega, Quinn ; Zhao, Yi ; Chao, Hanna H.J. ; Seasholtz, Audrey F. ; Dixon, Jack E. / Glial cell line-derived neurotrophic factor signals through the RET receptor and activates mitogen-activated protein kinase. In: Journal of Biological Chemistry. 1996 ; Vol. 271, No. 39. pp. 23619-23622.
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Glial cell line-derived neurotrophic factor signals through the RET receptor and activates mitogen-activated protein kinase. / Worby, Carolyn A.; Vega, Quinn; Zhao, Yi; Chao, Hanna H.J.; Seasholtz, Audrey F.; Dixon, Jack E.

In: Journal of Biological Chemistry, Vol. 271, No. 39, 10.10.1996, p. 23619-23622.

Research output: Contribution to journalArticleResearchpeer-review

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