Suppr超能文献

通过对接和分子动力学模拟鉴定Cdc25磷酸酶B中的喹啉二酮抑制剂结合位点。

Identification of the quinolinedione inhibitor binding site in Cdc25 phosphatase B through docking and molecular dynamics simulations.

作者信息

Ge Yushu, van der Kamp Marc, Malaisree Maturos, Liu Dan, Liu Yi, Mulholland Adrian J

机构信息

School of Life Sciences, University of Science and Technology of China, Hefei, 230027, People's Republic of China.

Centre of Computational Chemistry, School of Chemistry, University of Bristol, Bristol, BS8 1TS, UK.

出版信息

J Comput Aided Mol Des. 2017 Nov;31(11):995-1007. doi: 10.1007/s10822-017-0073-y. Epub 2017 Oct 9.

Abstract

Cdc25 phosphatase B, a potential target for cancer therapy, is inhibited by a series of quinones. The binding site and mode of quinone inhibitors to Cdc25B remains unclear, whereas this information is important for structure-based drug design. We investigated the potential binding site of NSC663284 [DA3003-1 or 6-chloro-7-(2-morpholin-4-yl-ethylamino)-quinoline-5, 8-dione] through docking and molecular dynamics simulations. Of the two main binding sites suggested by docking, the molecular dynamics simulations only support one site for stable binding of the inhibitor. Binding sites in and near the Cdc25B catalytic site that have been suggested previously do not lead to stable binding in 50 ns molecular dynamics (MD) simulations. In contrast, a shallow pocket between the C-terminal helix and the catalytic site provides a favourable binding site that shows high stability. Two similar binding modes featuring protein-inhibitor interactions involving Tyr428, Arg482, Thr547 and Ser549 are identified by clustering analysis of all stable MD trajectories. The relatively flexible C-terminal region of Cdc25B contributes to inhibitor binding. The binding mode of NSC663284, identified through MD simulation, likely prevents the binding of protein substrates to Cdc25B. The present results provide useful information for the design of quinone inhibitors and their mechanism of inhibition.

摘要

细胞周期蛋白依赖性激酶25磷酸酶B(Cdc25 phosphatase B)是癌症治疗的一个潜在靶点,可被一系列醌类化合物抑制。醌类抑制剂与Cdc25B的结合位点和模式尚不清楚,而这些信息对于基于结构的药物设计很重要。我们通过对接和分子动力学模拟研究了NSC663284 [DA3003-1或6-氯-7-(2-吗啉-4-基-乙氨基)-喹啉-5,8-二酮]的潜在结合位点。对接提示的两个主要结合位点中,分子动力学模拟仅支持其中一个位点用于抑制剂的稳定结合。先前提出的Cdc25B催化位点内及其附近的结合位点在50纳秒的分子动力学(MD)模拟中并未导致稳定结合。相比之下,C端螺旋和催化位点之间的一个浅口袋提供了一个显示出高稳定性的有利结合位点。通过对所有稳定的MD轨迹进行聚类分析,确定了两种相似的结合模式,其特征是蛋白质-抑制剂相互作用涉及Tyr428、Arg482、Thr547和Ser549。Cdc25B相对灵活的C端区域有助于抑制剂结合。通过MD模拟确定的NSC663284的结合模式可能会阻止蛋白质底物与Cdc25B结合。本研究结果为醌类抑制剂的设计及其抑制机制提供了有用信息。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验