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首页> 外文期刊>Cellular Signalling >Formyl peptide receptor-mediated ERK1/2 activation occurs through G(i) and is not dependent on beta-arrestin1/2
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Formyl peptide receptor-mediated ERK1/2 activation occurs through G(i) and is not dependent on beta-arrestin1/2

机译：甲酰基肽受体介导的ERK1 / 2活化通过G（I）发生，并且不依赖于β-instrin1 / 2

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摘要

Formyl peptide receptor (FPR) and C5a receptor (C5aR) are chemoattractant G protein-coupled receptors (GPCRs) involved in the innate immune response against bacterial infections and tissue injury. Like other GPCRs, they recruit beta-arrestin1/2 to the plasma membrane and activate the extracellular signal-regulated kinases 1 and 2 (ERK1/2). Previous studies with several GPCRs have suggested that beta-arrestins play an important role as signal transducers by scaffolding signaling molecules such as ERK1/2. This function of the beta-arrestins was not discovered until several years after their role in desensitization and endocytosis had been reported. In this study, we investigated the role of the beta-arrestins in the activation of ERK1/2 and receptor endocytosis. We took advantage of previously described mutants of FPR that have defects in G(i) coupling or beta-arrestin recruitment. The results obtained with the mutant FPRs, as well as experiments using an inhibitor of G(i) and cells overexpressing beta-arrestin2, showed that activation of ERK1/2 takes place through G(i) and is not affected by beta-arrestins. However, overexpression of beta-arrestin2 does enhance FPR sequestration from the cell surface, suggesting a role in desensitization, as shown for many other GPCRs. Experiments with CHO C5aR cells showed similar sensitivity to the G(i) inhibitor as CHO FPR cells, suggesting that the predominant activation of ERK1/2 through G protein may be a common characteristic among chemoattractant receptors. (C) 2007 Elsevier Inc. All rights reserved.
机译：甲醛肽受体（FPR）和C5A受体（C5AR）是涉及细菌感染和组织损伤的先天免疫应答的趋化蛋白偶联受体（GPCR）。与其他GPCR一样，它们募集β-instrin1 / 2至血浆膜并激活细胞外信号调节的激酶1和2（ERK1 / 2）。以前的几种GPCR的研究表明，Beta-Arectionins通过脚手架信号传导分子如ERK1 / 2来发挥重要作用。在据报道脱敏和内吞作用的作用后，迄今未发现该β-Arectrins的这种功能。在这项研究中，我们研究了β-arretins在激活ERK1 / 2和受体内吞作用中的作用。我们利用之前描述了FPR的突变体，其含有G（i）偶联或β-Arectrin招募。用突变FPRS获得的结果，以及使用G（i）的抑制剂和过表达β-inscrectin2的细胞的实验表明，ERK1 / 2的激活通过G（I）进行，并且不受β-interirins的影响。然而，Beta-Arcket2的过表达确实增强了来自细胞表面的FPR封存，表明在脱敏中的作用，如许多其他GPCR所示。 CHO C5AR细胞的实验表明与CHO FPR细胞的G（I）抑制剂类似的敏感性，表明ERK1 / 2至G蛋白的主要激活可能是培化剂受体中的共同特征。 （c）2007年elestvier Inc.保留所有权利。

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