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人血管加压素V2受体/激动剂复合物的分子模拟

Molecular modeling of the human vasopressin V2 receptor/agonist complex.

作者信息

Czaplewski C, Kaźmierkiewicz R, Ciarkowski J

机构信息

Faculty of Chemistry, University of Gdańsk, Poland.

出版信息

J Comput Aided Mol Des. 1998 May;12(3):275-87. doi: 10.1023/a:1007969526447.

Abstract

The V2 vasopressin renal receptor (V2R), which controls antidiuresis in mammals, is a member of the large family of heptahelical transmembrane (7TM) G protein-coupled receptors (GPCRs). Using the automated GPCR modeling facility available via Internet (http:/(/)expasy.hcuge.ch/swissmod/SWISS-MODEL.+ ++html) for construction of the 7TM domain in accord with the bovine rhodopsin (RD) footprint, and the SYBYL software for addition of the intra- and extracellular domains, the human V2R was modeled. The structure was further refined and its conformational variability tested by the use of a version of the Constrained Simulated Annealing (CSA) protocol developed in this laboratory. An inspection of the resulting structure reveals that the V2R (likewise any GPCR modeled this way) is much thicker and accordingly forms a more spacious TM cavity than most of the hitherto modeled GPCR constructs do, typically based on the structure of bacteriorhodopsin (BRD). Moreover, in this model the 7TM helices are arranged differently than they are in any BRD-based model. Thus, the topology and geometry of the TM cavity, potentially capable of receiving ligands, is in this model quite different than it is in the earlier models. In the subsequent step, two ligands, the native [arginine8]vasopressin (AVP) and the selective agonist [D-arginine8]vasopressin (DAVP) were inserted, each in two topologically non-equivalent ways, into the TM cavity and the resulting structures were equilibrated and their conformational variabilities tested using CSA as above. The best docking was selected and justified upon consideration of ligand-receptor interactions and structure-activity data. Finally, the amino acid residues were indicated, mainly in TM helices 3-7, as potentially important in both AVP and DAVP docking. Among those Cys112, Val115-Lys116, Gln119, Met123 in helix 3; Glu174 in helix 4; Val206, Ala210, Val213-Phe214 in helix 5; Trp284, Phe287-Phe288, Gln291 in helix 6; and Phe307, Leu310, Ala314 and Asn317 in helix 7 appeared to be the most important ones. Many of these residues are invariant for either the GPCR superfamily or the neurophyseal (vasopressin V2R, V1aR and V1bR and oxytocin OR) subfamily of receptors. Moreover, some of the equivalent residues in V1aR have already been found critical for the ligand affinity.

摘要

V2血管加压素肾受体(V2R)控制哺乳动物的抗利尿作用,是七螺旋跨膜(7TM)G蛋白偶联受体(GPCR)大家族的成员。利用通过互联网(http:/(/)expasy.hcuge.ch/swissmod/SWISS-MODEL.+ ++html)可获得的自动GPCR建模工具,根据牛视紫红质(RD)足迹构建7TM结构域,并使用SYBYL软件添加细胞内和细胞外结构域,对人V2R进行建模。通过使用本实验室开发的约束模拟退火(CSA)协议版本,对该结构进行进一步优化,并测试其构象变异性。对所得结构的检查表明,V2R(同样,任何以这种方式建模的GPCR)比大多数迄今建模的GPCR构建体(通常基于细菌视紫红质(BRD)的结构)要厚得多,因此形成了一个更宽敞的跨膜腔。此外,在该模型中,7TM螺旋的排列方式与任何基于BRD的模型都不同。因此,该模型中潜在能够结合配体的跨膜腔的拓扑结构和几何形状与早期模型有很大不同。在后续步骤中,将两种配体,即天然的[精氨酸8]血管加压素(AVP)和选择性激动剂[D-精氨酸8]血管加压素(DAVP),以两种拓扑学上不等价的方式分别插入跨膜腔中,对所得结构进行平衡,并使用上述CSA测试其构象变异性。在考虑配体-受体相互作用和构效关系数据后,选择并论证了最佳对接方式。最后,指出了主要在跨膜螺旋3-7中的氨基酸残基,它们在AVP和DAVP对接中可能具有重要作用。其中,螺旋3中的Cys112、Val115-Lys116、Gln119、Met123;螺旋4中的Glu174;螺旋5中的Val206、Ala210、Val213-Phe214;螺旋6中的Trp284、Phe287-Phe288、Gln291;以及螺旋7中的Phe307、Leu310、Ala314和Asn317似乎是最重要的。这些残基中的许多对于GPCR超家族或神经垂体(血管加压素V2R、V1aR和V1bR以及催产素OR)受体亚家族而言是不变的。此外,已经发现V1aR中的一些等效残基对于配体亲和力至关重要。

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