Trks: Signal transduction and intracellular pathways

Laura J. Klesse, Luis F. Parada

Research output: Contribution to journalArticle

130 Citations (Scopus)

Abstract

The neurotrophin family of growth factors supports survival and differentiation of neurons in the developing vertebrate nervous system by binding activating receptor tyrosine kinases, the Trks. Activation of Trk receptors leads to stimulation of a number of intracellular signaling cascades including, among others, the ras/extracellular regulated kinase (erk) and the phosphatidylinositol-3 kinase (PI 3 kinase) cascades. Over the past several years, work in several neurotrophin responsive systems has begun to identify the role each of these signaling cascades plays in the cellular response to neurotrophins. It now appears that neurotrophins, in particular nerve growth factor (NGF), mediate their multiple effects through a number of distinct intracellular signaling cascades. In this review, we will overview the evidence implicating specific signaling cascades in aspects of the cellular response to the neurotrophins, specifically in response to activation of TrkA by NGF.

Original languageEnglish (US)
Pages (from-to)210-216
Number of pages7
JournalMicroscopy Research and Technique
Volume45
Issue number4-5
DOIs
StatePublished - May 15 1999

Fingerprint

Signal transduction
neurotrophins
Nerve Growth Factors
signal transduction
Signal Transduction
cascades
nerve growth factor
nerves
Nerve Growth Factor
phosphotransferases (kinases)
Chemical activation
Phosphatidylinositol 3-Kinase
activation
nervous system
vertebrates
receptors
tyrosine
phosphatidylinositol 3-kinase
Receptor Protein-Tyrosine Kinases
Neurology

Keywords

  • Nerve growth factor
  • Neurons
  • PC12 cells
  • PI 3 kinase
  • Ras

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Anatomy
  • Instrumentation

Cite this

Trks : Signal transduction and intracellular pathways. / Klesse, Laura J.; Parada, Luis F.

In: Microscopy Research and Technique, Vol. 45, No. 4-5, 15.05.1999, p. 210-216.

Research output: Contribution to journalArticle

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