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本文引用的文献

1
Targeted Elimination of G Proteins and Arrestins Defines Their Specific Contributions to Both Intensity and Duration of G Protein-coupled Receptor Signaling.对G蛋白和抑制蛋白的靶向消除确定了它们对G蛋白偶联受体信号强度和持续时间的特定贡献。
J Biol Chem. 2016 Dec 30;291(53):27147-27159. doi: 10.1074/jbc.M116.754887. Epub 2016 Nov 16.
2
Functional competence of a partially engaged GPCR-β-arrestin complex.部分结合的 G 蛋白偶联受体-β-arrestin 复合物的功能能力。
Nat Commun. 2016 Nov 9;7:13416. doi: 10.1038/ncomms13416.
3
GPCR-G Protein-β-Arrestin Super-Complex Mediates Sustained G Protein Signaling.G蛋白偶联受体-G蛋白-β-抑制蛋白超级复合物介导持续的G蛋白信号传导。
Cell. 2016 Aug 11;166(4):907-919. doi: 10.1016/j.cell.2016.07.004. Epub 2016 Aug 4.
4
Monitoring G protein-coupled receptor and β-arrestin trafficking in live cells using enhanced bystander BRET.使用增强型旁观者 BRET 监测活细胞中的 G 蛋白偶联受体和β-arrestin 转运。
Nat Commun. 2016 Jul 11;7:12178. doi: 10.1038/ncomms12178.
5
Phospho-selective mechanisms of arrestin conformations and functions revealed by unnatural amino acid incorporation and (19)F-NMR.通过非天然氨基酸掺入和(19)F-NMR揭示的抑制蛋白构象和功能的磷酸选择性机制
Nat Commun. 2015 Sep 8;6:8202. doi: 10.1038/ncomms9202.
6
2D Projection Analysis of GPCR Complexes by Negative Stain Electron Microscopy.利用负染电子显微镜对G蛋白偶联受体复合物进行二维投影分析
Methods Mol Biol. 2015;1335:29-38. doi: 10.1007/978-1-4939-2914-6_3.
7
Crystal structure of rhodopsin bound to arrestin by femtosecond X-ray laser.通过飞秒X射线激光获得的视紫红质与抑制蛋白结合的晶体结构。
Nature. 2015 Jul 30;523(7562):561-7. doi: 10.1038/nature14656. Epub 2015 Jul 22.
8
Phenotypic regulation of the sphingosine 1-phosphate receptor miles apart by G protein-coupled receptor kinase 2.G蛋白偶联受体激酶2对1-磷酸鞘氨醇受体进行远距离表型调控。
Biochemistry. 2015 Jan 27;54(3):765-75. doi: 10.1021/bi501061h. Epub 2015 Jan 15.
9
Crystal structure of a common GPCR-binding interface for G protein and arrestin.G蛋白和阻遏蛋白共同的GPCR结合界面的晶体结构。
Nat Commun. 2014 Sep 10;5:4801. doi: 10.1038/ncomms5801.
10
Visualization of arrestin recruitment by a G-protein-coupled receptor.G 蛋白偶联受体介导的 arrestin 募集的可视化
Nature. 2014 Aug 14;512(7513):218-222. doi: 10.1038/nature13430. Epub 2014 Jun 22.

G蛋白偶联受体(GPCR)-β抑制蛋白复合物的不同构象介导脱敏、信号传导和内吞作用。

Distinct conformations of GPCR-β-arrestin complexes mediate desensitization, signaling, and endocytosis.

作者信息

Cahill Thomas J, Thomsen Alex R B, Tarrasch Jeffrey T, Plouffe Bianca, Nguyen Anthony H, Yang Fan, Huang Li-Yin, Kahsai Alem W, Bassoni Daniel L, Gavino Bryant J, Lamerdin Jane E, Triest Sarah, Shukla Arun K, Berger Benjamin, Little John, Antar Albert, Blanc Adi, Qu Chang-Xiu, Chen Xin, Kawakami Kouki, Inoue Asuka, Aoki Junken, Steyaert Jan, Sun Jin-Peng, Bouvier Michel, Skiniotis Georgios, Lefkowitz Robert J

机构信息

Department of Medicine, Duke University Medical Center, Durham, NC 27710.

Department of Biochemistry, Duke University Medical Center, Durham, NC 27710.

出版信息

Proc Natl Acad Sci U S A. 2017 Mar 7;114(10):2562-2567. doi: 10.1073/pnas.1701529114. Epub 2017 Feb 21.

DOI:10.1073/pnas.1701529114
PMID:28223524
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5347553/
Abstract

β-Arrestins (βarrs) interact with G protein-coupled receptors (GPCRs) to desensitize G protein signaling, to initiate signaling on their own, and to mediate receptor endocytosis. Prior structural studies have revealed two unique conformations of GPCR-βarr complexes: the "tail" conformation, with βarr primarily coupled to the phosphorylated GPCR C-terminal tail, and the "core" conformation, where, in addition to the phosphorylated C-terminal tail, βarr is further engaged with the receptor transmembrane core. However, the relationship of these distinct conformations to the various functions of βarrs is unknown. Here, we created a mutant form of βarr lacking the "finger-loop" region, which is unable to form the core conformation but retains the ability to form the tail conformation. We find that the tail conformation preserves the ability to mediate receptor internalization and βarr signaling but not desensitization of G protein signaling. Thus, the two GPCR-βarr conformations can carry out distinct functions.

摘要

β-抑制蛋白(βarrs)与G蛋白偶联受体(GPCRs)相互作用,使G蛋白信号脱敏,自身启动信号传导,并介导受体内吞作用。先前的结构研究揭示了GPCR-βarr复合物的两种独特构象:“尾部”构象,其中βarr主要与磷酸化的GPCR C末端尾部偶联;以及“核心”构象,除了磷酸化的C末端尾部外,βarr还与受体跨膜核心进一步结合。然而,这些不同构象与βarrs各种功能之间的关系尚不清楚。在这里,我们创建了一种缺乏“指环”区域的βarr突变形式,该区域无法形成核心构象,但保留了形成尾部构象的能力。我们发现,尾部构象保留了介导受体内化和βarr信号传导的能力,但不能使G蛋白信号脱敏。因此,两种GPCR-βarr构象可以执行不同的功能。