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Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells.


ABSTRACT: Atherogenesis involves activation of NF-kappaB 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-kappaB subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-kappaB-dependent gene. NF-kappaB activation by TNF-alpha or hydrogen peroxide was FAK independent. Events upstream of NF-kappaB, including integrin activation, Rac activation, reactive oxygen production, and degradation of IkappaB, were FAK independent. FAK therefore regulates NF-kappaB phosphorylation and transcriptional activity in response to flow by a novel mechanism.

SUBMITTER: Petzold T 

PROVIDER: S-EPMC2770750 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature

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Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells.

Petzold Tobias T   Orr A Wayne AW   Hahn Cornelia C   Jhaveri Krishna A KA   Parsons J Thomas JT   Schwartz Martin Alexander MA  

American journal of physiology. Cell physiology 20090708 4


Atherogenesis involves activation of NF-kappaB 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-kappaB subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-kappaB-dependent gene. NF-kappaB activation by TNF-alpha or hydrogen peroxide was FAK independent. Ev  ...[more]

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