Department of Biochemistry & Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Nat Commun. 2022 Apr 27;13(1):2269. doi: 10.1038/s41467-022-29927-9.
Protein-protein and protein-nucleic acid interactions are often considered difficult drug targets because the surfaces involved lack obvious druggable pockets. Cryptic pockets could present opportunities for targeting these interactions, but identifying and exploiting these pockets remains challenging. Here, we apply a general pipeline for identifying cryptic pockets to the interferon inhibitory domain (IID) of Ebola virus viral protein 35 (VP35). VP35 plays multiple essential roles in Ebola's replication cycle but lacks pockets that present obvious utility for drug design. Using adaptive sampling simulations and machine learning algorithms, we predict VP35 harbors a cryptic pocket that is allosterically coupled to a key dsRNA-binding interface. Thiol labeling experiments corroborate the predicted pocket and mutating the predicted allosteric network supports our model of allostery. Finally, covalent modifications that mimic drug binding allosterically disrupt dsRNA binding that is essential for immune evasion. Based on these results, we expect this pipeline will be applicable to other proteins.
蛋白质-蛋白质和蛋白质-核酸相互作用通常被认为是难以成药的靶点,因为涉及的表面缺乏明显的可成药口袋。隐匿口袋可能为靶向这些相互作用提供机会,但识别和利用这些口袋仍然具有挑战性。在这里,我们将一种用于识别隐匿口袋的通用方法应用于埃博拉病毒病毒蛋白 35(VP35)的干扰素抑制结构域(IID)。VP35 在埃博拉病毒的复制周期中发挥多种重要作用,但缺乏为药物设计提供明显用途的口袋。使用自适应采样模拟和机器学习算法,我们预测 VP35 具有一个隐匿口袋,该口袋与关键的 dsRNA 结合界面呈变构偶联。硫醇标记实验证实了预测的口袋,并且预测的变构网络的突变支持我们的变构模型。最后,模拟药物结合变构的共价修饰会破坏 dsRNA 结合,dsRNA 结合对于免疫逃逸至关重要。基于这些结果,我们预计该方法将适用于其他蛋白质。