Chen Zhewei, Liu Lu, Cattin Jerome, Knowles Tuomas P J, Bernardes Gonçalo J L
Yusuf Hamied Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, U.K.
Transition Bio, Ltd., Cambridge CB2 8DU, U.K.
J Am Chem Soc. 2025 Aug 13;147(32):28558-28563. doi: 10.1021/jacs.5c06625. Epub 2025 Aug 2.
Small-molecule modulation of biomolecular condensates has emerged as a novel and attractive therapeutic modality. Increasing evidence implicates dysregulated condensate formation in neurodegenerative diseases and cancer. However, the proteins that mediate condensate formation are typically difficult to drug directly with small molecules. Here, we present a charge-driven strategy and demonstrate its implementation on Ras GTPase-activating protein-binding protein 1 (G3BP1) to inhibit G3BP1-mediated stress granule (SG) formation. Small-molecule SG inhibitors were developed from the carbonylacrylic amide covalent functionality and were used to modify the folded domain of G3BP1 with surface charges, leading to an alteration of the conformational dynamics of intrinsically disordered regions. Cellular experiments using HeLa cells expressing cysteine-mutated G3BP1, together with structure-activity relationship studies, support the proposed charge-driven mechanism of action. Molecular dynamics simulations further suggest that the small-molecule G3BP1 modification promotes a shift toward more compact conformations, comparable to that induced by an ∼26% increase in IDR1-IDR3 interaction. Together, our findings establish a new strategy for the rational modulation of biomolecular condensates.
生物分子凝聚物的小分子调控已成为一种新颖且有吸引力的治疗方式。越来越多的证据表明,凝聚物形成失调与神经退行性疾病和癌症有关。然而,介导凝聚物形成的蛋白质通常很难直接用小分子药物进行靶向治疗。在此,我们提出一种电荷驱动策略,并展示其在Ras GTP酶激活蛋白结合蛋白1(G3BP1)上的应用,以抑制G3BP1介导的应激颗粒(SG)形成。小分子SG抑制剂由羰基丙烯酸酰胺共价官能团开发而来,并用于通过表面电荷修饰G3BP1的折叠结构域,从而改变内在无序区域的构象动力学。使用表达半胱氨酸突变型G3BP1的HeLa细胞进行的细胞实验,以及构效关系研究,支持了所提出的电荷驱动作用机制。分子动力学模拟进一步表明,小分子对G3BP1的修饰促进了向更紧凑构象的转变,类似于IDR1-IDR3相互作用增加约26%所诱导的转变。总之,我们的研究结果确立了一种合理调控生物分子凝聚物的新策略。