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This thesis examines the role of focal adhesion kinase (FAK) in vascular smooth muscle cell (SMC) migration. The author conditionally depletes FAK in cultured SMCs using adenoviral Cre infection. Depletion of FAK inhibits SMC migration in 3D assays, without affecting growth or apoptosis. While platelet-derived growth factor (PDGF)-induced membrane ruffling is intact, cell polarization is reduced fivefold in FAK-depleted SMCs. The author finds that FAK promotes localization of the formin Dia2 to focal adhesions and regulates RhoA/myosin light chain signaling. A novel interaction is also identified between Dia2 and the actin regulator cortactin






















































































