Ilter Metehan, Escorcia Andrés M, Schulze-Niemand Eric, Naumann Michael, Stein Matthias
Molecular Simulations and Design Group, Max Planck Institute for Dynamics of Complex Technical Systems, Sandtorstrasse 1, 39106 Magdeburg, Germany.
Institute for Experimental Internal Medicine, Medical Faculty, Otto von Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany.
J Chem Inf Model. 2025 Jan 27;65(2):921-936. doi: 10.1021/acs.jcim.4c01964. Epub 2025 Jan 9.
Cezanne-2 (Cez2) is a deubiquitinylating (DUB) enzyme involved in the regulation of ubiquitin-driven cellular signaling and selectively targets Lys11-linked polyubiquitin chains. As a representative member of the ovarian tumor (OTU) subfamily DUBs, it performs cysteine proteolytic isopeptide bond cleavage; however, its exact catalytic mechanism is not yet resolved. In this work, we used different computational approaches to get molecular insights into the Cezanne-2 catalytic mechanism. Extensive molecular dynamics (MD) simulations were performed for 12 μs to model free Cez2 and the diubiquitin (diUb) substrate-bound protein-protein complex in two different charge states of Cez2, each corresponding to a distinct reactive state in its catalytic cycle. The simulations were analyzed in terms of the relevant structural parameters for productive enzymatic catalysis. Reactive diUb-Cez2 complex configurations were identified, which lead to isopeptide bond cleavage and stabilization of the tetrahedral oxyanion intermediate. The reliability of these complexes was further assessed by quantum mechanics/molecular mechanics (QM/MM) optimizations. The results show that Cez2 follows a modified cysteine protease mechanism involving a catalytic Cys210/His367 dyad, with the oxyanion hole to be a part of the "C-loop," and polarization of His367 by the formation of a strictly conserved water bridge with Glu173. The third residue has a dual role in catalysis as it mediates substrate binding and polarization of the catalytic dyad. A similar mechanism was identified for Cezanne-1, the paralogue of Cez2. In general, our simulations provide valuable molecular information that may help in the rational design of selective inhibitors of Cez2 and closely related enzymes.
塞尚 - 2(Cez2)是一种去泛素化(DUB)酶,参与泛素驱动的细胞信号调节,并且选择性地作用于与赖氨酸11连接的多聚泛素链。作为卵巢肿瘤(OTU)亚家族DUB的代表性成员,它进行半胱氨酸蛋白水解异肽键切割;然而,其确切的催化机制尚未得到解决。在这项工作中,我们使用了不同的计算方法来深入了解塞尚 - 2的催化机制。进行了长达12微秒的广泛分子动力学(MD)模拟,以模拟处于两种不同电荷状态的游离Cez2以及与二聚泛素(diUb)底物结合的蛋白质 - 蛋白质复合物,每种电荷状态对应其催化循环中的一个不同反应状态。根据生产性酶催化的相关结构参数对模拟结果进行了分析。确定了反应性diUb - Cez2复合物构型,该构型导致异肽键断裂和四面体氧阴离子中间体的稳定。通过量子力学/分子力学(QM/MM)优化进一步评估了这些复合物的可靠性。结果表明,Cez2遵循一种经过修饰的半胱氨酸蛋白酶机制,涉及催化性的半胱氨酸210/组氨酸367二元组,氧阴离子孔是“C环”的一部分,并且通过与谷氨酸173形成严格保守的水桥使组氨酸367极化。第三个残基在催化中具有双重作用,因为它介导底物结合和催化二元组的极化。在Cez2的旁系同源物塞尚 - 1中也发现了类似的机制。总体而言,我们的模拟提供了有价值的分子信息,可能有助于合理设计Cez2及密切相关酶的选择性抑制剂。