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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
Summary
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.