FAK integrates growth-factor and integrin signals to promote cell migration

@article{Sieg2000FAKIG,
  title={FAK integrates growth-factor and integrin signals to promote cell migration},
  author={David J. Sieg and Christof R. Hauck and Du{\vs}ko Ili{\'c} and Candice K. Klingbeil and Erik M. Schaefer and Caroline H. Damsky and David D. Schlaepfer},
  journal={Nature Cell Biology},
  year={2000},
  volume={2},
  pages={249-256}
}
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… 
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Pyk2 and FAK regulate neurite outgrowth induced by growth factors and integrins
TLDR
It is shown that co-stimulation of growth-factor receptors and integrins activates the focal-adhesion kinase (FAK) family to promote outgrowth of neurites in PC12 and SH-SY5Y cells.
Focal Adhesion Kinase Facilitates Platelet-derived Growth Factor-BB-stimulated ERK2 Activation Required for Chemotaxis Migration of Vascular Smooth Muscle Cells*
TLDR
The results show that FAK inhibition by FRNK expression may provide a novel approach to regulate abnormal vascular SMC migration in vivo.
Matrix survival signaling: from fibronectin via focal adhesion kinase to c-Jun NH(2)-terminal kinase.
TLDR
It is reported that binding of the SH3 domain of p130Cas to proline-rich region 1 of FAK is required to support survival of fibroblasts on fibronectin when serum is withdrawn, and survival signals from extracellular matrix and serum are transduced by FAK via two distinct pathways.
Receptor Association to the Cytoskeleton and Integrins by Activating Src-Focal Adhesion Kinase and Induces Clustering of HER 2 β Transforming Growth Factor
TLDR
Data suggest that, by activating Src-FAK, TGF-B integrates ErbB receptor and integrin signaling to induce cell migration and survival during breast cancer progression.
MEK Kinase 1 Interacts with Focal Adhesion Kinase and Regulates Insulin Receptor Substrate-1 Expression*
TLDR
Findings indicate that MEKK1 interacts with FAK in focal adhesions and regulates IRS-1 expression, which appears to be physiologically relevant.
Control of motile and invasive cell phenotypes by focal adhesion kinase.
Direct Interaction of Focal Adhesion Kinase (FAK) with Met Is Required for FAK To Promote Hepatocyte Growth Factor-Induced Cell Invasion
TLDR
It is reported that FAK directly interacts with the hepatocyte growth factor receptor c-Met, providing evidence that constitutive Met-FAK interaction may be a critical determinant for tumor cells to acquire invasive potential.
Transforming growth factor beta induces clustering of HER2 and integrins by activating Src-focal adhesion kinase and receptor association to the cytoskeleton.
TLDR
Transforming growth factor beta induced focal adhesion kinase-dependent clustering of HER2 and integrins alpha(6), beta(1), and beta(4) in HER2-overexpressing mammary epithelial cells without altering the total and surface levels of Her2 receptors.
Focal adhesion kinase and its signaling pathways in cell migration and angiogenesis.
Matrix Survival Signaling
TLDR
It is reported that binding of the SH3 domain of p130Cas to proline-rich region 1 of FAK is required to support survival of fibroblasts on fibronectin when serum is withdrawn, and survival signals from extracellular matrix and serum are transduced by FAK via two distinct pathways.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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