Given the central position of the focal adhesion complex, both physically in coupling
integrins to the interstitium and biochemically in providing an upstream site for anabolic
signal generation, we asked whether the recruitment of non-receptor tyrosine kinases to the
cytoskeleton might be a mechanism whereby cellular loading could activate growth
regulatory signals responsible for cardiac hypertrophy. Analysis revealed cytoskeletal
association of c-Src, FAK, and β3-integrin, but no Fyn, in the pressure-overloaded right …