由乌比奎丁驱动的G蛋白合受体在内体的炎症信号传递
Norton Cheng1,2, Julio M Pimentel1, JoAnn Trejo1
1Department of Pharmacology, School of Medicine, University of California, San Diego, California, United States.
American journal of physiology. Cell physiology
|April 22, 2024
概括
在内分泌体上G蛋白结合受体 (GPCRs) 的ubiquitination启动了炎症信号. 这一过程涉及p38基因激活激酶通路,突出显示了GPCR翻译后修饰的新型作用.
科学领域:
- 细胞生物学 细胞生物学
- 分子信号传输的方法
- 免疫学 免疫学 免疫学
背景情况:
- G蛋白结合受体 (GPCR) 是关键的细胞表面蛋白质,调解生理反应.
- GPCRs的信号不仅来自于血,还来自于细胞内部分,如内分泌体.
- GPCRs经历翻译后的修改,包括酸化和无处不在,影响其功能和贩运.
研究的目的:
- 审查关于GPCR无化在细胞内信号传递中的作用的新兴发现.
- 突出了在调节GPCR介导的内分细胞的炎症反应的功能.
主要方法:
- 关于GPCR信号传递,贩运和无处不在的最新研究的文献综述.
- 专注于内体GPCR信号通路,包括G蛋白和β-arrestin相互作用.
- 检查GPCR无化在启动细胞内信号复合体中的作用.
主要成果:
- GPCR有能力从细胞内,特别是内分泌体中传递信号.
- 在内皮细胞中GPCRs的ubiquitination触发了p38基因激活激酶信号复合物的组装.
- 这种依赖于无处不在的信号复合体促进源自内分泌体的炎症反应.
结论:
- GPCR无化在启动内分泌体的炎症信号传递中起着关键作用.
- 内体GPCR信号传递是调节炎症反应的关键机制.
- 乌比基因化代表了GPCRs超越它们在受体贩运中的作用之外的新型监管机制.
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