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Signaling through focal adhesion kinase

D D Schlaepfer1, C R Hauck, D J Sieg

  • 1Scripps Research Institute, Department of Immunology, La Jolla, CA 92037, USA. dschlaep@scripps.edu

Progress in Biophysics and Molecular Biology
|June 4, 1999
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for cell growth, survival, and migration by linking integrin receptors to intracellular signals. FAK

Area of Science:

  • Cellular signaling and molecular biology
  • Integrin signaling pathways
  • Protein-tyrosine kinase functions

Background:

  • Integrin receptors mediate cell adhesion and transmit signals.
  • Focal adhesion kinase (FAK) is a key protein-tyrosine kinase (PTK) involved in integrin signaling.
  • FAK links integrin engagement to intracellular pathways regulating cell behavior.

Purpose of the Study:

  • To review the functions of FAK in linking integrin receptors to intracellular signaling.
  • To discuss FAK's role in cell growth, survival, migration, and tumor invasion.
  • To examine FAK activation mechanisms, substrate phosphorylation, and structural domains.

Main Methods:

  • Review of existing literature on FAK and integrin signaling.
  • Analysis of FAK's association with signaling proteins (e.g., Src-family PTKs, p130Cas, PI 3-kinase).
  • Discussion of FAK knockout fibroblast studies and FAK re-expression experiments.

Main Results:

  • FAK associates with multiple signaling proteins, forming a network for integrin-stimulated pathways.
  • FAK activation leads to downstream signaling, including ERK and JNK/MAPK pathways.
  • FAK knockout cells show deficits in cell migration, which are rescued by FAK re-expression.

Conclusions:

  • FAK is essential for regulating cell morphology and promoting cell migration.
  • FAK plays a significant role in generating cell survival signals.
  • FAK is implicated in promoting an invasive phenotype in human tumors.

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