Siess W, Grünberg B
Institut für Prophylaxe und Epidemiologie, Universität München, F.R.G.
Cell Signal. 1993 Mar;5(2):209-14. doi: 10.1016/0898-6568(93)90071-s.
The functional consequence of cyclic AMP-dependent phosphorylation of rap1B for stimulus-induced platelet activation is not known. Platelets were pretreated with the stable prostacyclin-analogue iloprost and resuspended in plasma without iloprost. Western blot analysis showed that rap1B was completely converted into its phosphorylated form in the iloprost-pretreated platelets. Surprisingly, the platelets that contained phosphorylated rap1B were found to respond fully to activation by a wide variety of stimuli: aggregation upon stimulation by collagen, phorbol ester, vasopressin, ADP, epinephrine, and ATP-secretion from dense granules induced by collagen, thrombin-receptor activating peptide, vasopressin and phorbol ester were unchanged as compared to control. The results indicate that cyclic AMP-dependent phosphorylation of rap1B does not play a role in the inhibition of the various signal transduction pathways that lead to platelet aggregation and dense granule secretion.
环磷酸腺苷（cAMP）依赖性的rap1B磷酸化对刺激诱导的血小板活化的功能影响尚不清楚。血小板先用稳定的前列环素类似物伊洛前列素预处理，然后重悬于不含伊洛前列素的血浆中。蛋白质印迹分析表明，在伊洛前列素预处理的血小板中，rap1B完全转化为其磷酸化形式。令人惊讶的是，发现含有磷酸化rap1B的血小板对多种刺激的活化反应完全：胶原、佛波酯、血管加压素、ADP、肾上腺素刺激后聚集，与对照相比，胶原、凝血酶受体激活肽、血管加压素和佛波酯诱导的致密颗粒中ATP分泌未发生变化。结果表明，cAMP依赖性的rap1B磷酸化在抑制导致血小板聚集和致密颗粒分泌的各种信号转导途径中不起作用。
