Publikation: FAK integrates growth-factor and integrin signals to promote cell migration
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Here we show that cells lacking focal adhesion kinase (FAK) are refractory to motility signals from platelet-derived and epidermal growth factors (PDGF and EGF respectively), and that stable re-expression of FAK rescues these defects. FAK associates with activated PDGF- and EGF-receptor (PDGFR and EGFR) signalling complexes, and expression of the band-4.1-like domain at the FAK amino terminus is sufficient to mediate an interaction with activated EGFR. However, efficient EGF-stimulated cell migration also requires FAK to be targeted, by its carboxy-terminal domain, to sites of integrin-receptor clustering. Although the kinase activity of FAK is not needed to promote PDGF- or EGF-stimulated cell motility, kinase-inactive FAK is transphosphorylated at the indispensable Src-kinase-binding site, FAK Y397, after EGF stimulation of cells. Our results establish that FAK is an important receptor-proximal link between growth-factor-receptor and integrin signalling pathways.
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SIEG, David J., Christof R. HAUCK, Du ko ILIĆ, Candice K. KLINGBEIL, Erik SCHAEFER, Caroline H. DAMSKY, David D. SCHLAEPFER, 2000. FAK integrates growth-factor and integrin signals to promote cell migration. In: Nature Cell Biology. 2000, 2(5), pp. 249-257. ISSN 1465-7392. Available under: doi: 10.1038/35010517BibTex
@article{Sieg2000integ-8279, year={2000}, doi={10.1038/35010517}, title={FAK integrates growth-factor and integrin signals to promote cell migration}, number={5}, volume={2}, issn={1465-7392}, journal={Nature Cell Biology}, pages={249--257}, author={Sieg, David J. and Hauck, Christof R. and Ilić, Du ko and Klingbeil, Candice K. and Schaefer, Erik and Damsky, Caroline H. and Schlaepfer, David D.} }
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