作者: Richard Marais , Yvonne Light , Hugh F. Paterson , Clive S. Mason , Christopher J. Marshall
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摘要: It has previously been shown that maximal activation of Raf-1 is produced by synergistic signals from oncogenic Ras and activated tyrosine kinases. This synergy arises because Ras-GTP translocates to the plasma membrane where it becomes phosphorylated on residues 340 341 membrane-bound kinases (Marais, R., Light, Y., Paterson, H. F., Marshall, C. J. (1995) EMBO 14, 3136-3145). We have examined whether other two members Raf family, A-Raf B-Raf, are regulated in a similar way Raf-1. behaves like Raf-1, being weakly more strongly Src, these synergize give activation. B-Raf contrast alone not Src. These results show merely requires generate Ras-GTP, whereas together with lead their phosphorylation. may therefore be primary target Ras.