Yano K, Higashida H, Nozawa Y
FEBS Lett. 1985 Apr 22;183(2):235-9. doi: 10.1016/0014-5793(85)80784-5.
The addition of bradykinin to 32Pi-labeled neuroblastoma X glioma hybrid NG108-15 cells caused a substantial loss of radioactivity from phosphatidylinositol 4,5-bisphosphate (PI-4,5-P2). The bradykinin-induced hydrolysis of PI-4,5-P2 was almost equally observed even when extracellular Ca2+ was depleted with EGTA (100 microns). On the other hand, high K+ depolarization of the cells, which allows Ca2+ influx through voltage-dependent Ca2+ channels, failed to induce any significant decrease in the radioactivity of PI-4,5-P2. These data indicate that the bradykinin-stimulated PI-4,5-P2 hydrolysis in NG108-15 cells is independent of extracellular Ca2+ and also that PI-4,5-P2 hydrolysis is not stimulated by an elevation of intracellular Ca2+ concentration.
将缓激肽添加到用³²Pi标记的神经母细胞瘤X胶质瘤杂交细胞NG108 - 15中，会导致磷脂酰肌醇4,5 - 二磷酸（PI - 4,5 - P2）的放射性显著损失。即使在用EGTA（100微摩尔）耗尽细胞外Ca²⁺的情况下，缓激肽诱导的PI - 4,5 - P2水解也几乎同样明显。另一方面，细胞的高钾去极化允许Ca²⁺通过电压依赖性Ca²⁺通道流入，但未能诱导PI - 4,5 - P2的放射性有任何显著降低。这些数据表明，缓激肽刺激的NG108 - 15细胞中PI - 4,5 - P2水解与细胞外Ca²⁺无关，并且PI - 4,5 - P2水解也不会因细胞内Ca²⁺浓度升高而受到刺激。
