@article{oai:nagasaki-u.repo.nii.ac.jp:00016413,
 author = {Kanda, Shigeru and Miyata, Yasuyoshi and Kanetake, Hiroshi and Smithgall, Thomas E},
 issue = {16},
 journal = {Experimental cell research},
 month = {Oct},
 note = {Cell migration is regulated by focal adhesion (FA) turnover. Fibroblast growth factor-2 (FGF-2) induces FA disassembly in the murine brain capillary endothelial cell line IBE, leading to FGF-2-directed chemotaxis. We previously showed that activation of Src and Fes by FGF-2 was involved in chemotaxis of IBE cells. In this study, we examined the interplay between Src and Fes. FGF-2 treatment decreased the number of FA in IBE cells, but not in cells expressing dominant-negative Fes (denoted KE5-15 cells). FGF-2 induced the activation of Src and subsequent binding to and phosphorylation of Cas in IBE cells, but not in KE5-15 cells. Focal adhesion kinase (FAK) activation and tyrosine phosphorylation by Src were also delayed in KE5-15 cells compared to parental cells. FGF-2 induced activation of Src within FA in IBE cells, but not in KE5-15 cells. Downregulation of Fes or FAK using small interfering RNA diminished Src activation by FGF-2 within FA. These findings suggest that activation of Fes by FGF-2 enhances FAK-dependent activation of Src within FA, promoting FGF-2-induced disassembly of focal adhesions., Experimental cell research, 312(16), pp.3015-3022; 2006},
 pages = {3015--3022},
 title = {Fibroblast growth factor-2 induces the activation of Src through Fes, which regulates focal adhesion disassembly.},
 volume = {312},
 year = {2006}
}