FAK and PYK2/CAKbeta in the nervous system: a link between neuronal activity, plasticity and survival?

Trends Neurosci. 1999 Jun;22(6):257-63. doi: 10.1016/s0166-2236(98)01358-7.


A major aim of neurobiology today is to improve understanding of the signaling pathways that couple rapid events, such as the action potential and neurotransmitter release, to long-lasting changes in synaptic strength and increased neuronal survival. These adaptations involve interactions of neurons with other cells and with the extracellular matrix. They use, in part, the same molecular machinery that controls adhesion, motility or survival in non-neuronal cells. This machinery includes two homologous non-receptor tyrosine kinases, FAK and PYK2/CAKbeta, and the associated SRC-family tyrosine kinases. Specific brain isoforms of FAK with distinct properties are regulated by neurotransmitters, whereas PYK2/CAKbeta is highly sensitive to depolarization. The multiplicity of the pathways that can be activated by these tyrosine kinases indicates their importance in signal transduction in the adult brain.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adult
  • Animals
  • Brain / enzymology*
  • Cell Adhesion Molecules / metabolism*
  • Cell Survival / physiology
  • Focal Adhesion Kinase 1
  • Focal Adhesion Kinase 2
  • Focal Adhesion Protein-Tyrosine Kinases
  • Humans
  • In Vitro Techniques
  • Neural Pathways / physiology
  • Neuronal Plasticity / physiology*
  • Neurotransmitter Agents / biosynthesis
  • Protein Isoforms / biosynthesis
  • Protein Isoforms / metabolism
  • Protein-Tyrosine Kinases / metabolism*
  • Synaptic Transmission / physiology


  • Cell Adhesion Molecules
  • Neurotransmitter Agents
  • Protein Isoforms
  • Protein-Tyrosine Kinases
  • Focal Adhesion Kinase 1
  • Focal Adhesion Kinase 2
  • Focal Adhesion Protein-Tyrosine Kinases
  • PTK2 protein, human