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Temporal gradients in fluid shear stress have been shown to induce a proatherogenic phenotype in endothelial cells. The biomechanical mechanism(s) that enables the endothelium to respond to fluid shear stress requires rapid activation and signal transduction. The small G protein Ras has been identified as an early link between rapid mechanotransduction events and the effects of shear stress on downstream signal-transduction cascades. The aim of this study was to elucidate the upstream mechanotransduction signaling events mediating the rapid activation of Ras by fluid shear stress in human endothelial cells.

Rapid Activation of Ras by Fluid Flow Is Mediated by Gα q and Gβγ Subunits of Heterotrimeric G Proteins in Human Endothelial Cells

Rapid Activation of Ras by Fluid Flow Is Mediated by Gα _q and Gβγ Subunits of Heterotrimeric G Proteins in Human Endothelial Cells