Singh Jay K, Hutt Darren M, Tait Bradley, Guy Naihsuan C, Sivils Jeffrey C, Ortiz Nina R, Payan Ashley N, Komaragiri Shravan Kumar, Owens Jazzmin Jovonna, Culbertson David, Blair Laura J, Dickey Chad, Kuo Szu Yu, Finley Dan, Dyson H Jane, Cox Marc B, Chaudhary Jaideep, Gestwicki Jason E, Balch William E
Department of Molecular Medicine, Skaggs Institute of Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Brad Tait Enterprise LLC, 80 Christian Way, North Andover, MA 01845, USA.
Cell Chem Biol. 2020 Mar 19;27(3):292-305.e6. doi: 10.1016/j.chembiol.2020.01.008. Epub 2020 Feb 3.
Hsp90 plays an important role in health and is a therapeutic target for managing misfolding disease. Compounds that disrupt co-chaperone delivery of clients to Hsp90 target a subset of Hsp90 activities, thereby minimizing the toxicity of pan-Hsp90 inhibitors. Here, we have identified SEW04784 as a first-in-class inhibitor of the Aha1-stimulated Hsp90 ATPase activity without inhibiting basal Hsp90 ATPase. Nuclear magnetic resonance analysis reveals that SEW84 binds to the C-terminal domain of Aha1 to weaken its asymmetric binding to Hsp90. Consistent with this observation, SEW84 blocks Aha1-dependent Hsp90 chaperoning activities, including the in vitro and in vivo refolding of firefly luciferase, and the transcriptional activity of the androgen receptor in cell-based models of prostate cancer and promotes the clearance of phosphorylated tau in cellular and tissue models of neurodegenerative tauopathy. We propose that SEW84 provides a novel lead scaffold for developing therapeutic approaches to treat proteostatic disease.
热休克蛋白90(Hsp90)在维持健康方面发挥着重要作用,并且是治疗错误折叠疾病的一个治疗靶点。能够破坏共伴侣蛋白将客户蛋白递送至Hsp90的化合物靶向Hsp90活性的一个子集,从而将泛Hsp90抑制剂的毒性降至最低。在此,我们已鉴定出SEW04784是一种一流的Aha1刺激的Hsp90 ATP酶活性抑制剂,且不抑制基础Hsp90 ATP酶。核磁共振分析表明,SEW84与Aha1的C末端结构域结合,以削弱其与Hsp90的不对称结合。与该观察结果一致,SEW84阻断Aha1依赖性的Hsp90伴侣活性,包括萤火虫荧光素酶的体外和体内重折叠,以及前列腺癌基于细胞模型中雄激素受体的转录活性,并在神经退行性tau病的细胞和组织模型中促进磷酸化tau的清除。我们提出,SEW84为开发治疗蛋白质稳态疾病的治疗方法提供了一种新型先导支架。