Fuchs P, Gruber E, Gitelman J, Kohn A
J Cell Physiol. 1980 May;103(2):271-8. doi: 10.1002/jcp.1041030212.
Adsorption of Sendai virus to HeLa cells induced in them an increased permeability to K+, Na+, Ca++, deoxyglucose, but not to fluorescein. The stimulation of uptake of 42K was temperature-dependent, did not occur below 15 degrees C, and was not inhibited by ouabain. The virus-induced increase in the uptake and release of 42K and of 3H deoxyglucose could not be mimicked by treatment of cells with linoleic acid, a procedure which increased the fluidity of the cellular membranes. The stimulatory effect of 0.5 mM ATP on the release of deoxyglucose was enhanced several fold in the presence of Sendai virus. These results seem to indicate the possible involvement of membranal enzymes such as e.g. protein kinase in the permeability changes induced by Sendai virus.
仙台病毒吸附到HeLa细胞上会使其对K⁺、Na⁺、Ca²⁺、脱氧葡萄糖的通透性增加,但对荧光素的通透性不变。42K摄取的刺激是温度依赖性的,在15摄氏度以下不发生,且不受哇巴因抑制。用亚油酸处理细胞(该过程增加了细胞膜的流动性)无法模拟病毒诱导的42K和3H脱氧葡萄糖摄取与释放的增加。在仙台病毒存在的情况下,0.5 mM ATP对脱氧葡萄糖释放的刺激作用增强了几倍。这些结果似乎表明,膜酶如蛋白激酶可能参与了仙台病毒诱导的通透性变化。