Delorenzo R J, Greengard P
Proc Natl Acad Sci U S A. 1973 Jun;70(6):1831-5. doi: 10.1073/pnas.70.6.1831.
Adenosine 3':5'-monophosphate (cyclic AMP) caused a decrease in the net rate of incorporation of radioactive phosphate into a specific protein (protein D) in a membrane fraction from toad bladder. Moreover, when the membrane protein was prelabeled with radioactive phosphate, cyclic AMP caused an increase in the net rate of removal of radioactive phosphate from this specific protein. Certain agents were shown to be selective inhibitors of membrane-bound protein D kinase or protein D phosphatase. With the help of these agents, it was concluded that cyclic AMP caused the activation of membrane-bound protein D phosphatase. The present data, together with earlier studies, are compatible with the possibility that the cyclic AMP-induced activation of a membrane-bound phosphoprotein phosphatase in toad bladder, with the consequent dephosphorylation of protein D, may be responsible for the physiological effects of antidiuretic hormone on sodium and/or water transport in this tissue.
3':5'-环磷酸腺苷(环磷腺苷)导致从蟾蜍膀胱膜分离物中放射性磷酸盐掺入特定蛋白质(蛋白质D)的净速率降低。此外,当膜蛋白用放射性磷酸盐预先标记时,环磷腺苷导致该特定蛋白质中放射性磷酸盐的净去除速率增加。某些试剂被证明是膜结合蛋白D激酶或蛋白D磷酸酶的选择性抑制剂。借助这些试剂,得出结论:环磷腺苷导致膜结合蛋白D磷酸酶的激活。目前的数据与早期研究一起,支持这样一种可能性,即环磷腺苷诱导蟾蜍膀胱中膜结合磷蛋白磷酸酶的激活,从而导致蛋白质D的去磷酸化,这可能是抗利尿激素对该组织中钠和/或水转运的生理作用的原因。