Murray A W, Froscio M
School of Biological Sciences, Flinders University of South Australia, Bedford Park, Australia.
Carcinogenesis. 1980 Aug;1(8):681-4. doi: 10.1093/carcin/1.8.681.
The tumor promotor 12-O-tetradecanoylphorbol-13-acetate (TPA) caused partial inhibition of the binding of [125I]epidermal growth factor ([125I]EGF) to intact mouse epidermal cells (HEL/37). The proportion of [125I]EGF binding which was insensitive to TPA inhibition decreased with increasing EGF concentration. The partial inhibition of [125I]EGF binding was not due to destruction of TPA or to covalent linkage of EGF to receptor sites. The binding of [125I]EGF to HEL/37 cells showed a curvilinear Scatchard plot; this was converted into a linear plot in the presence of TPA. We conclude that TPA acts to inhibit interactions between EGF receptors or between EGF receptors and some other membrane component(s).
肿瘤促进剂12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）对[125I]表皮生长因子（[125I]EGF）与完整小鼠表皮细胞（HEL/37）的结合产生部分抑制作用。对TPA抑制不敏感的[125I]EGF结合比例随EGF浓度增加而降低。[125I]EGF结合的部分抑制并非由于TPA的破坏或EGF与受体位点的共价连接。[125I]EGF与HEL/37细胞的结合呈现曲线型Scatchard图；在TPA存在下此图转变为线性图。我们得出结论，TPA的作用是抑制EGF受体之间或EGF受体与某些其他膜成分之间的相互作用。
