title: Rac[e] to the pole: setting up polarity in endothelial cells.
abstract: Mechanical forces influence many biological processes via activation of signaling molecules, including the family of Rho GTPases. Within the endothelium, the mechanical force of fluid shear stress regulates the spatiotemporal activation of Rho GTPases, including Rac1. Shear stress-induced Rac1 activation is required for numerous essential biological processes, including changes in permeability, alignment of the actin cytoskeleton, redox signaling, and changes in gene expression. Thus, identifying mechanisms of Rac1 activation and the spatial cues that direct proper localization of the GTPase is essential in order to gain a comprehensive understanding the role of Rac1 in shear stress responses. This commentary will highlight our current understanding of how Rac1 activity is regulated in response to shear stress, as well as the downstream consequences of Rac1 activation.
authors.affiliation: Department of Cell Biology and Physiology; University of North Carolina at Chapel Hill; Chapel Hill, NC USA.
authors.forename: Caitlin
authors.initials: C
authors.lastname: Collins
authors.affiliation: Department of Cell Biology and Physiology; University of North Carolina at Chapel Hill; Chapel Hill, NC USA.
authors.forename: Ellie
authors.initials: E
authors.lastname: Tzima
mesh_terms: D008841:Actin Cytoskeleton; D016764:Cell Polarity; D042783:Endothelial Cells / Q000378:metabolism*; D006801:Humans; D040542:Mechanotransduction, Cellular; D033081:Shear Strength; D020744:rac GTP-Binding Proteins / Q000378:metabolism*; D020830:rac1 GTP-Binding Protein / Q000378:metabolism
chemical_list: D020744:rac GTP-Binding Proteins; D020830:rac1 GTP-Binding Protein
keywords: Rac1; mechanotransduction; polarity; shear stress