Skip to main content
. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: Microvasc Res. 2011 Apr 22;83(1):12–21. doi: 10.1016/j.mvr.2011.04.005

Figure 4. Model of potential cross talk between PKCδ, p190, and FAK.

Figure 4

Under basal conditions, PKCδ functions to maintain endothelial barrier function through maintenance of a static level of RhoA activation and stimulation of FAK autophosphorylation. This allows for focal adhesion stabilization and organization of actin stress fibers. PKCδ-mediated activation of RhoA appears to occur independently of its effects on p190 phosphorylation.