Varsányi M, Behle G, Schäfer M
Z Naturforsch C J Biosci. 1986 Mar;41(3):310-4. doi: 10.1515/znc-1986-0311.
Vanadate increases the initial phosphatidylinositolphosphate formation rate as well as the steady state level of the above lipid phosphate when phosphatidylinositol associated with the isolated Ca2+ transport ATPase is phosphorylated either by the membrane bound endogeneously present phosphatidylinositol-kinase or by exogeneously added lipid kinase. Employing an ultrasonicated mixture of pure phosphatidylinositol and Triton X 100 (without membrane proteins) no vanadate effect can be seen. This vanadate effect is probably not mediated through the lipid kinase activity, but more likely, through conformational changes of the Ca2+ transport ATPase protein. Such conformational changes would lead to a higher degree of phosphatidylinositol exposed on the Ca2+ transport ATPase and thus a higher substrate concentration. Consequently, the initial phosphatidylinositolphosphate formation rate and steady state level increase.
当与分离的Ca2+转运ATP酶相关的磷脂酰肌醇被膜结合的内源性磷脂酰肌醇激酶或外源添加的脂质激酶磷酸化时，钒酸盐会增加初始磷脂酰肌醇磷酸的形成速率以及上述脂质磷酸的稳态水平。使用纯磷脂酰肌醇和Triton X 100的超声混合物（无膜蛋白）时，看不到钒酸盐的作用。钒酸盐的这种作用可能不是通过脂质激酶活性介导的，而更可能是通过Ca2+转运ATP酶蛋白的构象变化介导的。这种构象变化会导致更多的磷脂酰肌醇暴露在Ca2+转运ATP酶上，从而使底物浓度更高。因此，初始磷脂酰肌醇磷酸的形成速率和稳态水平增加。
