Nesterov A M, Sorokin A B, Okulova A N, Nikol'skiĭ N N
Tsitologiia. 1987 Aug;29(8):911-6.
In contrast to the intact EGF, a cyanogen bromide derivative of EGF (EGF-CNBr) does not induce an increase in uridine phosphorylation rate in 3T3 cells, the ability of the EGF-CNBr to stimulate autophosphorylation of the EGF-receptor in A-431 cells being reserved. EGF and EGF-CNBr were used in concentrations promoting their equivalent binding with EGF receptor in both the series of experiments, which was necessary because of a decreased affinity to binding EGF-CNBr. Thus, the EGF-induced receptor autophosphorylation was not enough for uridine kinase activation. The differences between EGF and EGF-CNBr cellular processing made it possible to discuss potential ways of uridine-kinase activity regulation during the early period of stimulation of quiescent cell cultures.
与完整的表皮生长因子（EGF）相反，EGF的溴化氰衍生物（EGF-CNBr）不会诱导3T3细胞中尿苷磷酸化速率增加，而EGF-CNBr刺激A-431细胞中EGF受体自身磷酸化的能力得以保留。在这一系列实验中，EGF和EGF-CNBr的使用浓度能促进它们与EGF受体的等效结合，由于EGF-CNBr的结合亲和力降低，这一点是必要的。因此，EGF诱导的受体自身磷酸化不足以激活尿苷激酶。EGF和EGF-CNBr细胞处理方式的差异使得人们能够讨论在静止细胞培养物刺激早期尿苷激酶活性调节的潜在途径。
