Baukrowitz T, Hwang T C, Nairn A C, Gadsby D C
Laboratory of Cardiac/Membrane Physiology, Rockefeller University, New York, New York 10021.
Neuron. 1994 Mar;12(3):473-82. doi: 10.1016/0896-6273(94)90206-2.
For cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels to open, they must be phosphorylated by protein kinase A and then exposed to a hydrolyzable nucleoside triphosphate, such as ATP. To test whether channel opening is linked to ATP hydrolysis, we applied VO4 and BeF3 to CFTR channels in inside-out patches excised from cardiac myocytes. These inorganic phosphate analogs interrupt ATP hydrolysis cycles by binding tightly in place of the released hydrolysis product, inorganic phosphate. The analogs acted only on CFTR channels opened by ATP and locked them open, increasing their mean open time by 2-3 orders of magnitude. These findings establish that opening and closing of CFTR channels are coupled to an ATP hydrolysis cycle.
对于囊性纤维化跨膜传导调节因子（CFTR）氯离子通道而言，其开放必须先被蛋白激酶A磷酸化，然后暴露于一种可水解的核苷三磷酸，如ATP。为了测试通道开放是否与ATP水解相关联，我们将VO4和BeF3应用于从心肌细胞上切下的内向外膜片中的CFTR通道。这些无机磷酸盐类似物通过紧密结合取代释放的水解产物无机磷酸盐来中断ATP水解循环。这些类似物仅作用于由ATP打开的CFTR通道并使其保持开放状态，将其平均开放时间增加了2 - 3个数量级。这些发现证实CFTR通道的开放和关闭与ATP水解循环相关联。
