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蛋白质精氨酸甲基转移酶1催化机制的理论见解。

Theoretical insights into catalytic mechanism of protein arginine methyltransferase 1.

作者信息

Zhang Ruihan, Li Xin, Liang Zhongjie, Zhu Kongkai, Lu Junyan, Kong Xiangqian, Ouyang Sisheng, Li Lin, Zheng Yujun George, Luo Cheng

机构信息

State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.

出版信息

PLoS One. 2013 Aug 20;8(8):e72424. doi: 10.1371/journal.pone.0072424. eCollection 2013.

Abstract

Protein arginine methyltransferase 1 (PRMT1), the major arginine asymmetric dimethylation enzyme in mammals, is emerging as a potential drug target for cancer and cardiovascular disease. Understanding the catalytic mechanism of PRMT1 will facilitate inhibitor design. However, detailed mechanisms of the methyl transfer process and substrate deprotonation of PRMT1 remain unclear. In this study, we present a theoretical study on PRMT1 catalyzed arginine dimethylation by employing molecular dynamics (MD) simulation and quantum mechanics/molecular mechanics (QM/MM) calculation. Ternary complex models, composed of PRMT1, peptide substrate, and S-adenosyl-methionine (AdoMet) as cofactor, were constructed and verified by 30-ns MD simulation. The snapshots selected from the MD trajectory were applied for the QM/MM calculation. The typical SN2-favored transition states of the first and second methyl transfers were identified from the potential energy profile. Deprotonation of substrate arginine occurs immediately after methyl transfer, and the carboxylate group of E144 acts as proton acceptor. Furthermore, natural bond orbital analysis and electrostatic potential calculation showed that E144 facilitates the charge redistribution during the reaction and reduces the energy barrier. In this study, we propose the detailed mechanism of PRMT1-catalyzed asymmetric dimethylation, which increases insight on the small-molecule effectors design, and enables further investigations into the physiological function of this family.

摘要

蛋白质精氨酸甲基转移酶1(PRMT1)是哺乳动物中主要的精氨酸不对称二甲基化酶,正逐渐成为癌症和心血管疾病的潜在药物靶点。了解PRMT1的催化机制将有助于抑制剂的设计。然而,PRMT1甲基转移过程和底物去质子化的详细机制仍不清楚。在本研究中,我们通过分子动力学(MD)模拟和量子力学/分子力学(QM/MM)计算,对PRMT1催化的精氨酸二甲基化进行了理论研究。构建了由PRMT1、肽底物和作为辅因子的S-腺苷甲硫氨酸(AdoMet)组成的三元复合物模型,并通过30纳秒的MD模拟进行了验证。从MD轨迹中选择的快照用于QM/MM计算。从势能剖面图中确定了第一次和第二次甲基转移的典型SN2倾向过渡态。底物精氨酸的去质子化在甲基转移后立即发生,E144的羧基作为质子受体。此外,自然键轨道分析和静电势计算表明,E144促进了反应过程中的电荷重新分布并降低了能垒。在本研究中,我们提出了PRMT1催化不对称二甲基化的详细机制,这增加了对小分子效应物设计的了解,并能够进一步研究该家族的生理功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6980/3748068/930518f7a79f/pone.0072424.g001.jpg

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