Brinkmeier H, Jockusch H
Developmental Biology Unit, University of Bielefeld, Fed. Rep. Germany.
Biochem Biophys Res Commun. 1987 Nov 13;148(3):1383-9. doi: 10.1016/s0006-291x(87)80285-1.
Certain phorbol esters and bryostatin 1, known activators of protein kinase C, were found to induce, in genetically normal muscle, an electrical membrane instability leading to unscheduled series of action potentials. Like in hereditary myotonias of man, goat and mouse, these symptoms were caused by a drastically lowered sarcolemmal chloride conductance. Our results indicate that the chloride channels of mammalian muscle may be subject to modulation by the protein kinase C-diacylglycerol system.
某些佛波酯和苔藓抑素1（已知的蛋白激酶C激活剂）被发现可在基因正常的肌肉中诱导膜电不稳定，导致一系列异常的动作电位。与人类、山羊和小鼠的遗传性肌强直一样，这些症状是由肌膜氯化物电导急剧降低引起的。我们的结果表明，哺乳动物肌肉的氯化物通道可能受蛋白激酶C - 二酰基甘油系统的调节。
