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通过综合计算研究深入了解 SENP1 Q597A 突变对 SUMO1 水解反应的别构效应。

Insights into the Allosteric Effect of SENP1 Q597A Mutation on the Hydrolytic Reaction of SUMO1 via an Integrated Computational Study.

机构信息

Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.

Department of Urology, Second Affiliated Hospital of Navy Medical University, Shanghai 200433, China.

出版信息

Molecules. 2022 Jun 28;27(13):4149. doi: 10.3390/molecules27134149.

Abstract

Small ubiquitin-related modifier (SUMO)-specific protease 1 (SENP1) is a cysteine protease that catalyzes the cleavage of the C-terminus of SUMO1 for the processing of SUMO precursors and deSUMOylation of target proteins. SENP1 is considered to be a promising target for the treatment of hepatocellular carcinoma (HCC) and prostate cancer. SENP1 Gln597 is located at the unstructured loop connecting the helices α4 to α5. The Q597A mutation of SENP1 allosterically disrupts the hydrolytic reaction of SUMO1 through an unknown mechanism. Here, extensive multiple replicates of microsecond molecular dynamics (MD) simulations, coupled with principal component analysis, dynamic cross-correlation analysis, community network analysis, and binding free energy calculations, were performed to elucidate the detailed mechanism. Our MD simulations showed that the Q597A mutation induced marked dynamic conformational changes in SENP1, especially in the unstructured loop connecting the helices α4 to α5 which the mutation site occupies. Moreover, the Q597A mutation caused conformational changes to catalytic Cys603 and His533 at the active site, which might impair the catalytic activity of SENP1 in processing SUMO1. Moreover, binding free energy calculations revealed that the Q597A mutation had a minor effect on the binding affinity of SUMO1 to SENP1. Together, these results may broaden our understanding of the allosteric modulation of the SENP1-SUMO1 complex.

摘要

小泛素相关修饰酶(SUMO)特异性蛋白酶 1(SENP1)是一种半胱氨酸蛋白酶,可催化 SUMO1 羧基末端的裂解,用于 SUMO 前体的加工和靶蛋白的去 SUMO 化。SENP1 被认为是治疗肝细胞癌(HCC)和前列腺癌的有前途的靶点。SENP1 的 Gln597 位于连接螺旋 α4 到 α5 的无规卷曲环上。SENP1 的 Q597A 突变通过未知机制使 SUMO1 的水解反应发生变构破坏。在此,通过广泛的微秒分子动力学(MD)模拟,与主成分分析、动态互相关分析、社区网络分析和结合自由能计算相结合,来阐明详细的机制。我们的 MD 模拟表明,Q597A 突变诱导 SENP1 发生明显的动态构象变化,特别是突变位点所在的连接螺旋 α4 到 α5 的无规卷曲环。此外,Q597A 突变导致活性位点的催化半胱氨酸残基 C603 和组氨酸残基 H533 发生构象变化,这可能会损害 SENP1 加工 SUMO1 的催化活性。此外,结合自由能计算表明,Q597A 突变对 SUMO1 与 SENP1 的结合亲和力影响较小。综上所述,这些结果可能会拓宽我们对 SENP1-SUMO1 复合物变构调节的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5e2/9268427/482bc0b96acc/molecules-27-04149-g001.jpg

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