State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Key Laboratory of Medical Data Analysis and Statistical Research of Tianjin, Nankai University, Tianjin 300353, China.
Int J Mol Sci. 2021 Jul 2;22(13):7185. doi: 10.3390/ijms22137185.
SMYD3 is a SET-domain-containing methyltransferase that catalyzes the transfer of methyl groups onto lysine residues of substrate proteins. Methylation of MAP3K2 by SMYD3 has been implicated in Ras-driven tumorigenesis, which makes SMYD3 a potential target for cancer therapy. Of all SMYD family proteins, SMYD3 adopt a closed conformation in a crystal structure. Several studies have suggested that the conformational changes between the open and closed forms may regulate the catalytic activity of SMYD3. In this work, we carried out extensive molecular dynamics simulations on a series of complexes with a total of 21 μs sampling to investigate the conformational changes of SMYD3 and unveil the molecular mechanisms. Based on the C-terminal domain movements, the simulated models could be depicted in three different conformational states: the closed, intermediate and open states. Only in the case that both the methyl donor binding pocket and the target lysine-binding channel had bound species did the simulations show SMYD3 maintaining its conformation in the closed state, indicative of a synergetic effect of the cofactors and target lysine on regulating the conformational change of SMYD3. In addition, we performed analyses in terms of structure and energy to shed light on how the two regions might regulate the C-terminal domain movement. This mechanistic study provided insights into the relationship between the conformational change and the methyltransferase activity of SMYD3. The more complete understanding of the conformational dynamics developed here together with further work may lay a foundation for the rational drug design of SMYD3 inhibitors.
SMYD3 是一种 SET 结构域含有甲基转移酶,可催化将甲基基团转移到底物蛋白的赖氨酸残基上。SMYD3 对 MAP3K2 的甲基化作用与 Ras 驱动的肿瘤发生有关,这使得 SMYD3 成为癌症治疗的潜在靶点。在所有 SMYD 家族蛋白中,SMYD3 在晶体结构中采用封闭构象。有几项研究表明,开放和封闭形式之间的构象变化可能调节 SMYD3 的催化活性。在这项工作中,我们对一系列复合物进行了广泛的分子动力学模拟,总采样时间为 21 μs,以研究 SMYD3 的构象变化并揭示分子机制。基于 C 末端结构域的运动,模拟模型可以描绘为三种不同的构象状态:封闭、中间和开放状态。只有当甲基供体结合口袋和靶标赖氨酸结合通道都结合了物质时,模拟才显示 SMYD3 保持其封闭构象,这表明辅助因子和靶标赖氨酸对调节 SMYD3 构象变化具有协同作用。此外,我们还进行了结构和能量分析,以阐明这两个区域如何调节 C 末端结构域的运动。这项机制研究深入了解了 SMYD3 构象变化与甲基转移酶活性之间的关系。在这里开发的构象动力学的更完整理解,以及进一步的工作,可能为 SMYD3 抑制剂的合理药物设计奠定基础。