Shim Joong-Youn, Khurana Leepakshi, Kendall Debra A
Department of Chemistry, University of North Carolina, Chapel Hill, North Carolina, 27514.
Department of Pharmaceutical Sciences, University of Connecticut, Storrs, Connecticut, 06269-3092.
Proteins. 2016 Apr;84(4):532-43. doi: 10.1002/prot.24999. Epub 2016 Feb 15.
Despite the important role of the carboxyl-terminus (Ct) of the activated brain cannabinoid receptor one (CB1) in the regulation of G protein signaling, a structural understanding of interactions with G proteins is lacking. This is largely due to the highly flexible nature of the CB1 Ct that dynamically adapts its conformation to the presence of G proteins. In the present study, we explored how the CB1 Ct can interact with the G protein by building on our prior modeling of the CB1-Gi complex (Shim, Ahn, and Kendall, The Journal of Biological Chemistry 2013;288:32449-32465) to incorporate a complete CB1 Ct (Glu416(Ct)-Leu472(Ct)). Based on the structural constraints from NMR studies, we employed ROSETTA to predict tertiary folds, ZDOCK to predict docking orientation, and molecular dynamics (MD) simulations to obtain two distinct plausible models of CB1 Ct in the CB1-Gi complex. The resulting models were consistent with the NMR-determined helical structure (H9) in the middle region of the CB1 Ct. The CB1 Ct directly interacted with both Gα and Gβ and stabilized the receptor at the Gi interface. The results of site-directed mutagenesis studies of Glu416(Ct), Asp423(Ct), Asp428(Ct), and Arg444(Ct) of CB1 Ct suggested that the CB1 Ct can influence receptor-G protein coupling by stabilizing the receptor at the Gi interface. This research provided, for the first time, models of the CB1 Ct in contact with the G protein.
尽管活化的脑大麻素受体1(CB1)的羧基末端(Ct)在G蛋白信号调节中起着重要作用,但目前仍缺乏对其与G蛋白相互作用的结构理解。这主要是由于CB1 Ct具有高度的灵活性,能够根据G蛋白的存在动态调整其构象。在本研究中,我们基于之前构建的CB1 - Gi复合物模型(Shim、Ahn和Kendall,《生物化学杂志》2013年;288:32449 - 32465),纳入完整的CB1 Ct(Glu416(Ct)- Leu472(Ct)),探索CB1 Ct如何与G蛋白相互作用。基于核磁共振(NMR)研究的结构限制,我们使用ROSETTA预测三级折叠,ZDOCK预测对接方向,并通过分子动力学(MD)模拟获得CB1 - Gi复合物中CB1 Ct的两种不同的合理模型。所得模型与CB1 Ct中间区域由NMR确定的螺旋结构(H9)一致。CB1 Ct直接与Gα和Gβ相互作用,并在Gi界面处稳定受体。对CB1 Ct的Glu416(Ct)、Asp423(Ct)、Asp428(Ct)和Arg444(Ct)进行定点诱变研究的结果表明,CB1 Ct可通过在Gi界面处稳定受体来影响受体 - G蛋白偶联。本研究首次提供了CB1 Ct与G蛋白接触的模型。