作者: B. Li , M. Subleski , N. Fusaki , T. Yamamoto , T. Copeland
关键词:
摘要: mSOS, a guanine nucleotide exchange factor, is positive regulator of Ras. Fyn tyrosine protein kinase potential mediator in T-cell antigen receptor signal transduction subsets T cells. We investigated the functional and physical interaction between mSOS hybridoma Stimulation induced activation activity immunoprecipitates. Overexpression mutants with an activated mutation Src homology 2 deletion resulted stimulation suppression activity, respectively. The complex formations Fyn-Shc, Shc-Grb2, Grb2-mSOS were detected Fyn-transformed cells, whereas SH2 mutant failed to form mSOS. Moreover, phosphorylation Shc was by overexpression Fyn. These findings support idea that activates bound Grb2 through Shc. Unlike current prevailing model, Fyn-induced Ras might involve catalytic