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USP3: Key deubiquitylation enzyme in human diseases
Cancer Science ( IF 5.7 ) Pub Date : 2024-04-23 , DOI: 10.1111/cas.16178
Hongyan Zhang 1, 2 , Wenjing Liu 3 , Yingying Wu 4 , Ceshi Chen 3, 5
Affiliation  

Ubiquitination and deubiquitylation are pivotal posttranslational modifications essential for regulating cellular protein homeostasis and are implicated in the development of human diseases. Ubiquitin‐specific protease 3 (USP3), a member of the ubiquitin‐specific protease family, serves as a key deubiquitylation enzyme, playing a critical role in diverse cellular processes including the DNA damage response, cell cycle regulation, carcinogenesis, tumor cell proliferation, migration, and invasion. Despite notable research efforts, our current understanding of the intricate and context‐dependent regulatory networks governing USP3 remains incomplete. This review aims to comprehensively synthesize existing published works on USP3, elucidating its multifaceted roles, functions, and regulatory mechanisms, while offering insights for future investigations. By delving into the complexities of USP3, this review strives to provide a foundation for a more nuanced understanding of its specific roles in various cellular processes. Furthermore, the exploration of USP3's regulatory networks may uncover novel therapeutic strategies targeting this enzyme in diverse human diseases, thereby holding promising clinical implications. Overall, an in‐depth comprehension of USP3's functions and regulatory pathways is crucial for advancing our knowledge and developing targeted therapeutic approaches for human diseases.

中文翻译:

USP3:人类疾病中关键的去泛素化酶

泛素化和去泛素化是调节细胞蛋白质稳态所必需的关键翻译后修饰,与人类疾病的发展有关。泛素特异性蛋白酶 3 (USP3) 是泛素特异性蛋白酶家族的一员,作为关键的去泛素化酶,在多种细胞过程中发挥着关键作用,包括 DNA 损伤反应、细胞周期调节、癌变、肿瘤细胞增殖、迁徙、入侵。尽管进行了显着的研究工作,但我们目前对管理 USP3 的复杂且依赖于环境的监管网络的理解仍然不完整。本综述旨在全面综合现有已发表的 USP3 著作,阐明其多方面的作用、功能和监管机制,同时为未来的研究提供见解。通过深入研究 USP3 的复杂性,本综述致力于为更细致地了解其在各种细胞过程中的特定作用奠定基础。此外,对 USP3 调控网络的探索可能会发现针对多种人类疾病的这种酶的新治疗策略,从而具有良好的临床意义。总的来说,深入理解 USP3 的功能和调控途径对于提高我们的知识和开发人类疾病的靶向治疗方法至关重要。
更新日期:2024-04-23
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