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SUMO‐specific proteases: SENPs in oxidative stress‐related signaling and diseases
Biofactors ( IF 6 ) Pub Date : 2024-03-29 , DOI: 10.1002/biof.2055
Yaqi Jiao 1, 2 , Xiaojuan Zhang 3 , Zhenshan Yang 4
Affiliation  

Oxidative stress is employed to depict a series of responses detrimental to normal cellular functions resulting from an imbalance between intracellular oxidants, mainly reactive oxygen species and antioxidant defenses. Oxidative stress often contributes to the development of various diseases, including cancer, cardiovascular diseases, and neurodegenerative diseases. In this process, the relationship between small ubiquitin‐like modifier (SUMO) and oxidative stress has garnered significant attention, with its posttranslational modification (PTM) frequently serving as a marker of oxidative stress status. Sentrin/SUMO‐specific proteases (SENPs), affected by alternative splicing, PTMs such as phosphorylation and ubiquitination, and various protein interactions, are crucial molecules in the SUMO process. The human SENP family has six members (SENP1–3, SENP5–7), which are classified into two categories based on sequence similarity, substrate specificity, and subcellular location. They have two core functions in the human body: first, by cleaving the precursor SUMO and exposing the C‐terminal glycine, they initiate the SUMO process; second, they can specifically recognize and dissociate SUMO proteins bound to substrates, a process known as deSUMOylation. However, the connection between deSUMOylation and oxidative stress remains a relatively unexplored area despite their strong association with oxidative diseases such as cancer and cardiovascular disease. This article aims to illustrate the significant contribution of SENPs to the oxidative stress pathway through deSUMOylation by reviewing their structure and classification, their roles in oxidative stress, and the changes in their expression and activity in several typical oxidative stress‐related diseases.

中文翻译:

SUMO 特异性蛋白酶:氧化应激相关信号传导和疾病中的 SENP

氧化应激用于描述由于细胞内氧化剂(主要是活性氧)和抗氧化防御之间的不平衡而导致的一系列对正常细胞功能有害的反应。氧化应激通常会导致多种疾病的发生,包括癌症、心血管疾病和神经退行性疾病。在此过程中,小泛素样修饰剂(SUMO)与氧化应激之间的关系引起了人们的广泛关注,其翻译后修饰(PTM)经常作为氧化应激状态的标志。 Sentrin/SUMO 特异性蛋白酶 (SENP) 受选择性剪接、磷酸化和泛素化等 PTM 以及各种蛋白质相互作用的影响,是 SUMO 过程中的关键分子。人类 SENP 家族有 6 个成员(SENP1-3、SENP5-7),根据序列相似性、底物特异性和亚细胞位置分为两类。它们在人体内有两个核心功能:首先,通过裂解前体SUMO并暴露C端甘氨酸,启动SUMO过程;其次,它们可以特异性识别并解离与底物结合的 SUMO 蛋白,这一过程称为去 SUMO 化。然而,尽管去SUMO化和氧化应激与癌症和心血管疾病等氧化性疾病密切相关,但它们之间的联系仍然是一个相对未被探索的领域。本文旨在通过回顾SENPs的结构和分类、它们在氧化应激中的作用以及它们在几种典型氧化应激相关疾病中表达和活性的变化,阐明SENPs通过去SUMOylation对氧化应激通路的重要贡献。
更新日期:2024-03-29
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