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PMID: 9069267 Published · ppublish English Journal Article Review

Signal transduction by the neurotrophin receptors.

Current opinion in cell biology ·Vol. 9 ·No. 2 ·1997-04-00 ·Pages 213-21

Kaplan DR, Miller FD

Abstract

The neurotrophins signal cell survival, differentiation, growth cessation, and apoptosis through two cell surface receptors, the Trks and p75NTR (p75 neurotrophin receptor). Recent advances indicate that the particular events that are mediated by neurotrophins are dependent upon the cell type and the expression pattern of each neurotrophin receptor. For example, TrkA activation induces cell death of neural tumor cells, and survival and differentiation of neurons. Likewise, p75NTR, when activated in the absence of a strong Trk signal, induces apoptosis of neurons, while in the presence of Trk it enhances responses to neurotrophin. These differing responses point to a complex interplay between neurotrophin-stimulated survival, differentiation, and apoptosis pathways.

MeSH Terms
Apoptosis Cell Differentiation Nerve Growth Factors/metabolism Neurons/metabolism Phosphatidylinositol 3-Kinases Phosphotransferases (Alcohol Group Acceptor)/metabolism Protein Serine-Threonine Kinases Proto-Oncogene Proteins/metabolism Proto-Oncogene Proteins c-akt Receptor, Nerve Growth Factor Receptors, Nerve Growth Factor/metabolism Signal Transduction ras Proteins/metabolism
Chemicals
Nerve Growth Factors Proto-Oncogene Proteins Receptor, Nerve Growth Factor Receptors, Nerve Growth Factor Phosphotransferases (Alcohol Group Acceptor) Protein Serine-Threonine Kinases Proto-Oncogene Proteins c-akt ras Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Kaplan D R
Brain Tumor Research Centre, Montreal Neurological Institute, 3801 University Street, Montreal, PQ, Canada, H3A 2B4. mcdv@musica.mcgill.ca
Miller F D
Article Info
Journal
Current opinion in cell biology
Abbr.
Curr Opin Cell Biol
ISSN
0955-0674
Published
1997-04-00
Pages
213-21
Language
English
Region
England
NLM ID
8913428
Subset
IM
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