N‐terminal cleavage fragment of focal adhesion kinase is required to activate the survival signalling pathway in cultured myoblasts under oxidative stress

摘要: We have previously shown that the cultured L6 myoblasts are susceptible to menadione-induced oxidative stress. Damaged cells were detached from culture dishes. In present study, we focused on focal adhesion kinase (FAK), which plays pivotal roles in maintaining function and cell survival. FAK, normally localized at regions of myoblasts, was not observed under stress induced by menadione H2O2. Two cleavage products, 80-kDa N-terminal FAK 35-kDa C-terminal fragments, as well full-length (125 kDa) detected normal conditions western blotting with anti-N-terminal or anti-C-terminal sera. Of interest finding products (but FAK) disappeared The inhibited calpeptin, a specific calpain inhibitor. addition, pre-incubation calpeptin resulted sharp decrease survival signals, such Akt phosphorylation ratio Bcl-2/Bax, conditions. By contrast, only relative viability, but also Bcl-2/Bax significantly improved when transfected DNA construct FAK-Myc. These results suggest positively regulates signalling early phases myoblasts.