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首页> 外文期刊>Developmental cell >Activation of G alpha i at the Golgi by GIV/Girdin Imposes Finiteness in Arf1 Signaling
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Activation of G alpha i at the Golgi by GIV/Girdin Imposes Finiteness in Arf1 Signaling

机译：GIV / Girdin在高尔基体上激活G alpha i赋予Arf1信号传导有限性

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摘要

A long-held tenet of heterotrimeric G protein signal transduction is that it is triggered by G protein-coupled receptors (GPCRs) at the PM. Here, we demonstrate that Gi is activated in the Golgi by GIV/Girdin, a non-receptor guanine-nucleotide exchange factor (GEF). GIV-dependent activation of Gi at the Golgi maintains the finiteness of the cyclical activation of ADP-ribosylation factor 1 (Arf1), a fundamental step in vesicle traffic in all eukaryotes. Several interactions with other major components of Golgi trafficking-e.g., active Arf1, its regulator, ArfGAP2/3, and the adaptor protein beta-COP-enable GIV to coordinately regulate Arf1 signaling. When the GIV-G alpha i pathway is selectively inhibited, levels of GTP-bound Arf1 are elevated and protein transport along the secretory pathway is delayed. These findings define a paradigm in non-canonical G protein signaling at the Golgi, which places GIV-GEF at the crossroads between signals gated by the trimeric G proteins and the Arf family of monomeric GTPases.
机译：异源三聚体G蛋白信号转导的长期宗旨是，它由PM处的G蛋白偶联受体（GPCR）触发。在这里，我们证明了GIV在Golgi中被GIV / Girdin（一种非受体鸟嘌呤核苷酸交换因子（GEF））激活。 GIV上Giv的GIV依赖性激活维持了ADP-核糖基化因子1（Arf1）循环激活的有限性，这是所有真核生物中囊泡运输的基本步骤。与高尔基体运输的其他主要组成部分的几种相互作用，例如活性Arf1，其调节剂ArfGAP2 / 3和使衔接蛋白β-COP激活的GIV协同调节Arf1信号传导。当GIV-Gα1途径被选择性抑制时，与GTP结合的Arf1的水平升高，并且沿分泌途径的蛋白运输被延迟。这些发现定义了高尔基体非经典G蛋白信号传导的范例，这将GIV-GEF置于三聚体G蛋白门控的信号与单体GTPases的Arf家族之间的十字路口。

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