Allosteric mechanisms underlie GPCR signaling to SH3-domain proteins through arrestin
Allosteric mechanisms underlie GPCR signaling to SH3-domain proteins through arrestin
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变构机制是 GPCR 通过抑制蛋白向 SH3 结构域蛋白发出信号的基础
DOI：
10.1038/s41589-018-0115-3
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发表时间：
2018-08
影响因子：
14.8
通讯作者：
Wang Jiangyun
中科院分区：
文献类型：
--
作者：
Yang Fan;Xiao Peng;Qu Chang-xiu;Liu Qi;Wang Liu-yang;Liu Zhi-xin;He Qing-tao;Liu Chuan;Xu Jian-ye;Li Rui-rui;Li Meng-jing;Li Qing;Guo Xu-zhen;Yang Zhao-ya;He Dong-fang;Yi Fan;Ruan Ke;Shen Yue-mao;Yu Xiao;Sun Jin-peng;Wang Jiangyun
来自800种G蛋白偶联受体（GPCRs）并传递至众多含SH3结构域蛋白（SH3 - CPs）的信号，对重要生理功能起着调节作用。这些GPCRs可能通过激动剂依赖性的抑制蛋白募集，向SH3 - CPs发出信号，从而共享一条通用途径。
不过，原文“rat”一词在此处似乎语义不通，可能是有误或不完整，你可以检查一下原文是否准确。
Signals from 800 G-protein-coupled receptors (GPCRs) to many SH3 domain-containing proteins (SH3-CPs) regulate important physiological functions. These GPCRs may share a common pathway by signaling to SH3-CPs via agonist-dependent arrestin recruitment rather than through direct interactions. In the present study,19F-NMR and cellular studies revealed that downstream of GPCR activation engagement of the receptor-phospho-tail with arrestin allosterically regulates the specific conformational states and functional outcomes of remote β-arrestin 1 proline regions (PRs). The observed NMR chemical shifts of arrestin PRs were consistent with the intrinsic efficacy and specificity of SH3 domain recruitment, which was controlled by defined propagation pathways. Moreover, in vitro reconstitution experiments and biophysical results showed that the receptor–arrestin complex promoted SRC kinase activity through an allosteric mechanism. Thus, allosteric regulation of the conformational states of β-arrestin 1 PRs by GPCRs and the allosteric activation of downstream effectors by arrestin are two important mechanisms underlying GPCR-to-SH3-CP signaling.
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影响因子：
64.5
作者：
Manglik A;Kim TH;Masureel M;Altenbach C;Yang Z;Hilger D;Lerch MT;Kobilka TS;Thian FS;Hubbell WL;Prosser RS;Kobilka BK
通讯作者：
Kobilka BK
影响因子：
64.8
作者：
Venkatakrishnan, A. J.;Deupi, Xavier;Lebon, Guillaume;Heydenreich, Franziska M.;Flock, Tilman;Miljus, Tamara;Balaji, Santhanam;Bouvier, Michel;Veprintsev, Dmitry B.;Tate, Christopher G.;Schertler, Gebhard F. X.;Babu, M. Madan
通讯作者：
Babu, M. Madan
DOI：
10.1126/science.1215802
发表时间：
2012-03-02
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Liu JJ;Horst R;Katritch V;Stevens RC;Wüthrich K
通讯作者：
Wüthrich K
抑制蛋白偏向的 AT1R 激动作用通过 TRPC3 偶联诱导急性儿茶酚胺分泌
影响因子：
16.6
作者：
Liu CH;Gong Z;Liang ZL;Liu ZX;Yang F;Sun YJ;Ma ML;Wang YJ;Ji CR;Wang YH;Wang MJ;Cui FA;Lin A;Zheng WS;He DF;Qu CX;Xiao P;Liu CY;Thomsen AR;Joseph Cahill T 3rd;Kahsai AW;Yi F;Xiao KH;Xue T;Zhou Z;Yu X;Sun JP
通讯作者：
Sun JP
影响因子：
64.8
作者：
Taniguchi, Koji;Wu, Li-Wha;Grivennikov, Sergei I.;de Jong, Petrus R.;Lian, Ian;Yu, Fa-Xing;Wang, Kepeng;Ho, Samuel B.;Boland, Brigid S.;Chang, John T.;Sandborn, William J.;Hardiman, Gary;Raz, Eyal;Maehara, Yoshihiko;Yoshimura, Akihiko;Zucman-Rossi, Jessica;Guan, Kun-Liang;Karin, Michael
通讯作者：
Karin, Michael