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The American Journal of Physiology - Cell Physiology
Year: 2009  |  Volume: 297  |  Issue: 4  |  Page No.: 814 - 822

Focal adhesion kinase modulates activation of NF-{kappa}B by flow in endothelial cells

T Petzold, A. W Orr, C Hahn, K. A Jhaveri, J. T Parsons and M. A. Schwartz    


Atherogenesis involves activation of NF-B in endothelial cells by fluid shear stress. Because this pathway involves integrins, we investigated the involvement of focal adhesion kinase (FAK). We found that FAK was not required for flow-stimulated translocation of the p65 NF-B subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-B-dependent gene. NF-B activation by TNF- or hydrogen peroxide was FAK independent. Events upstream of NF-B, including integrin activation, Rac activation, reactive oxygen production, and degradation of IB, were FAK independent. FAK therefore regulates NF-B phosphorylation and transcriptional activity in response to flow by a novel mechanism.

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