van der Valk J, Verlaan I, de Laat S W, Moolenaar W H
J Biol Chem. 1987 Feb 25;262(6):2431-4.
The transmembrane potential of Rous sarcoma virus (RSV)-infected Rat-1 cells, expressing the pp60v-src protein kinase, is markedly less negative (by approximately 30 mV) than that of their normal counterparts. By contrast, the membrane potential of Rat-1 cells infected with Kirsten sarcoma virus is virtually unaltered. The RSV-induced membrane depolarization is shown to be due to a severalfold increase in the cation permeability ratio (PNa/PK) of the plasma membrane. When cells infected with a temperature-sensitive mutant of RSV (ts LA29), encoding a src protein with heat-labile kinase activity, are shifted from the nonpermissive to the permissive temperature, a rapid and sustained membrane depolarization is observed. Conversely, thermal inactivation of the ts LA29 pp60v-src kinase activity rapidly restores the membrane potential to near normal levels. Addition of epidermal growth factor, platelet-derived growth factor, or insulin to uninfected cells fails to cause a detectable change in membrane potential. We conclude that, unlike growth factor receptor tyrosine kinases, pp60v-src can induce, either directly or indirectly, a major change in the membrane permeability to monovalent cations.
表达pp60v-src蛋白激酶的劳斯肉瘤病毒（RSV）感染的大鼠1细胞的跨膜电位，比其正常对应细胞的跨膜电位明显不那么负（约30 mV）。相比之下，感染柯斯顿肉瘤病毒的大鼠1细胞的膜电位几乎没有改变。RSV诱导的膜去极化表明是由于质膜阳离子通透性比率（PNa/PK）增加了几倍。当感染了编码具有热不稳定激酶活性的src蛋白的RSV温度敏感突变体（ts LA29）的细胞从非允许温度转变为允许温度时，观察到快速且持续的膜去极化。相反，ts LA29 pp60v-src激酶活性的热失活迅速将膜电位恢复到接近正常水平。向未感染的细胞中添加表皮生长因子、血小板衍生生长因子或胰岛素不会导致膜电位出现可检测到的变化。我们得出结论，与生长因子受体酪氨酸激酶不同，pp60v-src可以直接或间接诱导单价阳离子膜通透性的重大变化。
