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首页> 外文期刊>Journal of receptor and signal transduction research >Receptor-specific regulation of ERK1/2 activation by members of the 'free fatty acid receptor' family
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Receptor-specific regulation of ERK1/2 activation by members of the 'free fatty acid receptor' family

机译：“游离脂肪酸受体”家族成员对ERK1 / 2激活的受体特异性调节

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Context: The "free fatty acid receptors" (FFARs) GPR40, GPR41, and GPR43 regulate various physiological homeostases, and are all linked to activation of extracellular signal-regulated kinases (ERK)1/2. Objective: Investigation of coupling of FFARs to two other mitogen-activated protein kinases (MAPKs) sometimes regulated by G protein-coupled receptors (GPCRs), c-Jun N-terminal kinase (JNK) and p38MAPK, and characterization of signaling proteins involved in the regulation of FFAR-mediated ERK1/2 activation. Methods: FFARs were recombinantly expressed, cells challenged with the respective agonist, and MAPK activation quantitatively determined using an AlphaScreen SureFire assay. Inhibitors for signaling proteins were utilized to characterize ERK1/2 pathways. Results: Propionate-stimulated GPR41 strongly coupled to ERK1/2 activation, while the coupling of linoleic acid-activated GPR40 and acetate-activated GPR43 was weaker. JNK and p38MAPK were weakly activated by FFARs. All three receptors activated ERK1/2 fully or partially via Gi/o and Rac. PI3K was relevant for GPR40- and GPR41-mediated ERK1/2 activation, and Src was essential for GPR40- and GPR43-induced activation. Raf-1 was not involved in the GPR43-triggered activation. Conclusion: The results demonstrate a novel role of Rac in GPCR-mediated ERK1/2 signaling, and that GPCRs belonging to the same family can regulate ERK1/2 activation by different receptor-specific mechanisms.
机译：背景：“游离脂肪酸受体”（FFAR）GPR40，GPR41和GPR43调节各种生理稳态酶，并且都与细胞外信号调节激酶（ERK）1/2的激活有关。目的：研究FFARs与有时受G蛋白偶联受体（GPCR），c-Jun N端激酶（JNK）和p38MAPK调节的其他两种促分裂原活化蛋白激酶（MAPK）的偶联，以及涉及的信号蛋白的表征FFAR介导的ERK1 / 2激活的调控。方法：FFARs重组表达，用各自的激动剂攻击细胞，并使用AlphaScreen SureFire测定法定量测定MAPK活化。信号蛋白的抑制剂被用来表征ERK1 / 2途径。结果：丙酸酯刺激的GPR41与ERK1 / 2激活紧密耦合，而亚油酸激活的GPR40和乙酸盐激活的GPR43耦合较弱。 JNK和p38MAPK被FFARs弱激活。所有三种受体均通过Gi / o和Rac完全或部分激活ERK1 / 2。 PI3K与GPR40和GPR41介导的ERK1 / 2激活有关，而Src对于GPR40和GPR43诱导的激活至关重要。 Raf-1不参与GPR43触发的激活。结论：结果表明Rac在GPCR介导的ERK1 / 2信号转导中具有新作用，并且属于同一家族的GPCR可以通过不同的受体特异性机制调节ERK1 / 2的激活。

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