Multiple connections link FAK to cell motility and invasion

Curr Opin Genet Dev. 2004 Feb;14(1):92-101. doi: 10.1016/j.gde.2003.12.002.

Abstract

The ability of intracellular signaling networks to orchestrate a complex biological response such as cell motility requires that individual signaling proteins must act as integrators, responding to multiple extracellular inputs and regulating multiple signaling pathway outputs. In this review, we highlight recent findings that place focal adhesion kinase (FAK) in an important receptor-proximal position in the regulation of growth factor and integrin-stimulated cell motility. Emphasis is placed on the molecular mechanisms of FAK activation, connections of FAK to focal contact formation as well as turnover, and the potential that FAK function in promoting cell invasion may be distinct from its role in cell motility.

Publication types

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

MeSH terms

  • Cell Movement / physiology*
  • Enzyme Activation
  • Fibroblasts / physiology
  • Focal Adhesion Protein-Tyrosine Kinases
  • Integrins / physiology
  • Phosphorylation
  • Protein-Tyrosine Kinases / physiology*
  • Signal Transduction*

Substances

  • Integrins
  • Protein-Tyrosine Kinases
  • Focal Adhesion Protein-Tyrosine Kinases