Falasca M, Carvelli A, Iurisci C, Qiu R G, Symons M H, Corda D
Department of Cell Biology and Oncology, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Chieti, Italy.
Mol Biol Cell. 1997 Mar;8(3):443-53. doi: 10.1091/mbc.8.3.443.
Glycerophosphoinositols are phosphoinositide metabolites whose levels are constitutively elevated in Ras-transformed cells. Here, we show that one of these compounds, glycerophosphoinositol-4-phosphate (GroPIns-4-P) responds acutely to the stimulation of the epidermal growth factor receptor, with a fast, massive and transient increase. The mechanism leading to GroPIns-4-P formation involves the activation of phosphoinositide-3 kinase and the small GTP-binding protein Rac, since GroPIns-4-P was neither formed in cells expressing the dominant negative form of Rac nor in cells treated with the phosphoinositide-3 kinase inhibitor wortmannin. GroPIns-4-P has been previously shown to inhibit adenylyl cyclase. Accordingly, epidermal growth factor also decreased the basal, cholera toxin-stimulated, and forskolin-stimulated cyclic AMP levels with kinetics similar to those of GroPIns-4-P formation, suggesting that GroPIns-4-P mediates this inhibitory effect. The hormone-induced formation of GroPIns-4-P was detected in several cell lines of various origin, suggesting that GroPIns-4-P is a novel intracellular messenger of the Ras pathway, possibly able to convey information from tyrosine kinase receptors to the cyclic AMP cascade.
甘油磷酸肌醇是磷酸肌醇代谢产物,其水平在Ras转化细胞中持续升高。在此,我们表明这些化合物之一,甘油磷酸肌醇-4-磷酸(GroPIns-4-P)对表皮生长因子受体的刺激有急性反应,呈现快速、大量且短暂的增加。导致GroPIns-4-P形成的机制涉及磷酸肌醇-3激酶和小GTP结合蛋白Rac的激活,因为在表达Rac显性负性形式的细胞中或在用磷酸肌醇-3激酶抑制剂渥曼青霉素处理的细胞中均未形成GroPIns-4-P。先前已表明GroPIns-4-P可抑制腺苷酸环化酶。因此,表皮生长因子也降低了基础、霍乱毒素刺激和福斯高林刺激的环磷酸腺苷水平,其动力学与GroPIns-4-P形成的动力学相似,表明GroPIns-4-P介导了这种抑制作用。在多种来源的几种细胞系中均检测到激素诱导的GroPIns-4-P形成现象,这表明GroPIns-4-P是Ras途径的一种新型细胞内信使,可能能够将信息从酪氨酸激酶受体传递至环磷酸腺苷级联反应。