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泛素特异性蛋白酶7(USP7)的小分子变构激活剂。

Small-molecule allosteric activator of ubiquitin-specific protease 7 (USP7).

作者信息

Jaen Maisonet Isabella, Sharafi Mona, Korchak Emilie J, Salazar-Chaparro Andres, Bratt Ariana, Parikh Tvesha, Varca Anthony C, Shah Binita, Darnowski Michael, Chung Mia, Teh Wei Pin, Che Jianwei, Bezsonova Irina, Buhrlage Sara J

出版信息

bioRxiv. 2025 Mar 16:2025.03.14.643379. doi: 10.1101/2025.03.14.643379.

Abstract

Ubiquitin-specific protease 7 (USP7) is a deubiquitylase essential for cell homeostasis, DNA repair, and regulation of both tumor suppressors and oncogenes. Inactivating USP7 mutations have been associated with Hao-Fountain Syndrome (HAFOUS), a rare neurodevelopmental disorder. Although a range of USP7 inhibitors have been developed over the last decade, in the context of HAFOUS as well as oncogene regulation, USP7 activators may represent a more relevant approach. To address this challenge, we report the discovery and characterization of a small-molecule activator of USP7 called MS-8. We showed that MS-8 activates USP7 by engaging the allosteric C-terminal binding pocket of USP7, thus mimicking the allosteric autoactivation by the USP7 C-terminal tail. We observed that MS-8 engages and activates mutant USP7 in a cellular context, impacting downstream proteins. Taken together, our study provides validation of the USP7 activator that paves the way towards novel activation-driven USP7 pharmacology.

摘要

泛素特异性蛋白酶7(USP7)是一种去泛素化酶,对细胞稳态、DNA修复以及肿瘤抑制因子和癌基因的调控至关重要。USP7失活突变与郝-方丹综合征(HAFOUS)有关,这是一种罕见的神经发育障碍。尽管在过去十年中已经开发了一系列USP7抑制剂,但在HAFOUS以及癌基因调控的背景下,USP7激活剂可能是一种更合适的方法。为应对这一挑战,我们报告了一种名为MS-8的USP7小分子激活剂的发现和特性。我们表明,MS-8通过结合USP7的变构C末端结合口袋来激活USP7,从而模拟USP7 C末端尾巴的变构自激活。我们观察到,MS-8在细胞环境中结合并激活突变型USP7,影响下游蛋白质。综上所述,我们的研究验证了USP7激活剂,为新型激活驱动的USP7药理学铺平了道路。

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