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Coxsackievirus B3 entry into the host cell interferes with G-protein-mediated transmembrane signalling

机译:柯萨奇病毒B3进入宿主细胞会干扰G蛋白介导的跨膜信号传导

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In the present work we used various cell lines in order to study the possible effect of coxsackievirus B3 (CVB3) entry on the adenylyl cyclase transmembrane signalling system. A significant decrease (by about 10–20%) was found in forskolin-augmented as well as in AlF4?- and GTPγS-sensitive adenylyl cyclase activity in plasma membranes isolated from HeLa, HEp-2, Vero and green monkey kidney cells shortly (up to 60 min) preincubated with CVB3 (5 PFU/cell). Moreover, the ability of G-proteins derived from plasma membranes of infected cells to reconstitute AC activity in the cyc? mutant of S49 cells was also reduced. Content of G-protein subunits, however, remained unchanged after CVB3 attachment. Functional alterations in the G-protein-mediated adenylyl cyclase signalling system were accompanied by a marked decrease (by about 20–40%) of intracellular cAMP levels in virus-affected cells. These findings demonstrate clearly that CVB3 may affect functioning of the G-protein regulated adenylyl cyclase transmembrane signalling system in virus-sensitive cells as early as during the first period of its contact with the cellular plasma membrane.
机译:在当前的工作中,我们使用了各种细胞系来研究柯萨奇病毒B3(CVB3)进入对腺苷酸环化酶跨膜信号传导系统的可能影响。在从HeLa,HEp-2,Vero和绿猴肾细胞分离的质膜中,福司柯林增强以及AlF4α和GTPγS敏感的腺苷酸环化酶活性显着降低(约10–20%)(最多60分钟)与CVB3(5 PFU /细胞)预孵育。而且,来源于被感染细胞质膜的G蛋白在细胞中重构AC活性的能力。 S49细胞的突变体也减少了。然而,CVB3附着后,G蛋白亚基的含量保持不变。 G蛋白介导的腺苷酸环化酶信号传导系统的功能改变伴随着病毒感染细胞内细胞内cAMP水平的显着降低(约20–40%)。这些发现清楚地表明,CVB3可能最早在其与细胞质膜接触的第一阶段就影响病毒敏感细胞中G蛋白调节的腺苷酸环化酶跨膜信号传导系统的功能。

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