Activation of Src family kinases (SFK) and the subsequent phosphorylation of VE-cadherin
have been proposed as major regulatory steps leading to increases in vascular permeability
in response to inflammatory mediators and growth factors. To investigate Src signaling in the
absence of parallel signaling pathways initiated by growth factors or inflammatory mediators,
we activated Src and SFKs by expression of dominant negative Csk, expression of
constitutively active Src, or knockdown of Csk. Activation of SFK by overexpression of …