Stony Brook University Renaissance School of Medicine, Department of Pharmacological Sciences, Stony Brook, NY 11794, USA.
Antidote Health Foundation for Cure of Cancer, Cambridge, MA 02139, USA.
J Mol Biol. 2022 Sep 15;434(17):167628. doi: 10.1016/j.jmb.2022.167628. Epub 2022 May 17.
Allostery plays a primary role in regulating protein activity, making it an important mechanism in human disease and drug discovery. Identifying allosteric regulatory sites to explore their biological significance and therapeutic potential is invaluable to drug discovery; however, identification remains a challenge. Allosteric sites are often "cryptic" without clear geometric or chemical features. Since allosteric regulatory sites are often less conserved in protein kinases than the orthosteric ATP binding site, allosteric ligands are commonly more specific than ATP competitive inhibitors. We present a generalizable computational protocol to predict allosteric ligand binding sites based on unbiased ligand binding simulation trajectories. We demonstrate the feasibility of this protocol by revisiting our previously published ligand binding simulations using the first identified viral proto-oncogene, Src kinase, as a model system. The binding paths for kinase inhibitor PP1 uncovered three metastable intermediate states before binding the high-affinity ATP-binding pocket, revealing two previously known allosteric sites and one novel site. Herein, we validate the novel site using a combination of virtual screening and experimental assays to identify a V-type allosteric small-molecule inhibitor that targets this novel site with specificity for Src over closely related kinases. This study provides a proof-of-concept for employing unbiased ligand binding simulations to identify cryptic allosteric binding sites and is widely applicable to other protein-ligand systems.
变构作用在调节蛋白质活性方面起着主要作用,是人类疾病和药物发现中的重要机制。确定变构调节位点以探索其生物学意义和治疗潜力对于药物发现是非常有价值的;然而,鉴定仍然是一个挑战。变构位点通常没有明确的几何或化学特征,因此是“隐匿的”。由于变构调节位点在蛋白激酶中通常不如 orthosteric ATP 结合位点保守,因此变构配体通常比 ATP 竞争性抑制剂更具特异性。我们提出了一种基于无偏 ligand 结合模拟轨迹来预测变构配体结合位点的可推广计算方案。我们通过重新使用先前发表的配体结合模拟来验证该方案的可行性,使用首次鉴定的病毒原癌基因Src 激酶作为模型系统。激酶抑制剂 PP1 的结合路径在结合高亲和力 ATP 结合口袋之前揭示了三个亚稳态中间状态,揭示了两个先前已知的变构位点和一个新的位点。在此,我们使用虚拟筛选和实验测定的组合来验证新的位点,以鉴定一种针对该新型位点的 V 型变构小分子抑制剂,该抑制剂特异性针对 Src 而不是密切相关的激酶。这项研究为使用无偏 ligand 结合模拟来鉴定隐匿性变构结合位点提供了概念验证,并广泛适用于其他蛋白配体系统。