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白细胞介素-8的G蛋白偶联信号转导途径

G protein-coupled signal transduction pathways for interleukin-8.

作者信息

Wu D, LaRosa G J, Simon M I

机构信息

Division of Biology, California Institute of Technology, Pasadena 91125.

出版信息

Science. 1993 Jul 2;261(5117):101-3. doi: 10.1126/science.8316840.

Abstract

Interleukin-8 (IL-8) is one of the major mediators of the inflammatory response. The pathways by which IL-8 activates inositide-specific phospholipase C (PLC) were investigated by co-expression of different components of the guanosine triphosphate binding protein (G protein) pathway in COS-7 cells. Two distinct IL-8 receptors reconstituted ligand-dependent activation of endogenous PLC when transfected together with the G protein alpha subunits G alpha 14, G alpha 15, or G alpha 16. However, reconstitution was not observed with cells that overexpressed G alpha q or G alpha 11. Furthermore, IL-8 receptors interacted with endogenous pertussis toxin-sensitive G proteins or with the recombinant G protein Gi to release free beta gamma subunits that could then specifically activate the beta 2 isoform of PLC. These findings suggest that IL-8 acts through signal-transducing pathways that are limited to specific heterotrimeric G proteins and effectors. These may provide suitable targets for the development of anti-inflammatory agents.

摘要

白细胞介素-8(IL-8)是炎症反应的主要介质之一。通过在COS-7细胞中共表达鸟苷三磷酸结合蛋白(G蛋白)途径的不同组分,研究了IL-8激活肌醇特异性磷脂酶C(PLC)的途径。当与G蛋白α亚基Gα14、Gα15或Gα16一起转染时,两种不同的IL-8受体可重建内源性PLC的配体依赖性激活。然而,在过表达Gαq或Gα11的细胞中未观察到重建。此外,IL-8受体与内源性百日咳毒素敏感G蛋白或重组G蛋白Gi相互作用,释放游离的βγ亚基,然后这些亚基可特异性激活PLC的β2同工型。这些发现表明,IL-8通过限于特定异源三聚体G蛋白和效应器的信号转导途径发挥作用。这些可能为抗炎药物的开发提供合适的靶点。

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