Prostaglandin-E 1 - and Sodium Nitroprusside-Regulated Protein Phosphorylation in Platelets
Prostaglandin-E 1 - and Sodium Nitroprusside-Regulated Protein Phosphorylation in Platelets
复制标题
血小板中前列腺素 E 1 和硝普钠调节的蛋白质磷酸化
DOI：
10.1007/978-1-4757-0166-1_26
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
U. Walter
中科院分区：
文献类型：
--
作者：
M. Nieberding;R. Waldmann;U. Walter
多种药物如ADP、胶原、凝血酶、血小板激活因子(PAF)*和其他药物激活血小板时，伴随着肌球蛋白轻链(MR 20K)和一种明显MR为44 K1、2的可溶性蛋白的磷酸化增加。某些血管扩张剂，如cGMP提高剂(SNP、硝酸甘油)和cAMP提高剂(PGE1PGI2)能够抑制血小板的激活和激活相关蛋白的磷酸化1，2。由于CAK和CGK可能介导血小板内环核苷酸调节剂的作用，我们现在比较了在完整的血小板中观察到的血管扩张剂调节的蛋白磷酸化和在血小板膜上发现的环核苷酸刺激的蛋白磷酸化3，4。结果表明，至少有一种磷蛋白由SNP和PGE1刺激的蛋白磷酸化分别由CGK和CAK介导。
A variety of agents like ADP, collagen, thrombin, platelet-activating- factor (PAF)* and others activate platelets with a concomitant increase in the phosphorylation of myosin light chain (Mr 20 K) and of a soluble protein with apparent Mr of 44 K1,2. Certain vasodilators such as cGMP-elevating agents (SNP, nitroglycerin) and cAMP-elevating agents (PGE1PGI2) are able to inhibit platelet activation and the activation-associated protein phosphorylation1,2. Since cAK and cGK may mediate the effects of cyclic nucleotide-regulating agents in platelets, we have now compared the vasodilator-regulated protein phosphorylation observed in intact platelets with the cyclic nucleotide stimulated protein phosphorylation found in platelet membranes3,4. The results show for at least one phosphoprotein that the SNP-and PGE1-stimulated protein phosphorylation is mediated by cGK and cAK, respectively.