Figures & data
Figure 1 Proposed mechanism of AhR-dependent control of cell migration through interaction with Vav3 signaling. Under physiological cell conditions, AhR binds to the Vav3 promoter and regulates its constitute expression. Vav3 protein then serves as GDP/GTP exchange factor (GEF) for the small GTPases Rac1 and RhoA. Once in their GTP-bound form, Rac1 and RhoA modulate cell migration, plasma membrane protrusions and cytoskeleton reorganization. The inhibitory effect of high levels of Rac1 activity on RhoA-dependent control of stress fibers is considered (blunt arrow).
