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Review
. 2018 Jan 25;47(1):82-88.
doi: 10.3785/j.issn.1008-9292.2018.02.12.

[Protein ubiquitination on the regulation of inflammatory bowel disease]

[Article in Chinese]
Jing Ling  1 , Hongrui Li  1 , Weilin Chen  1   2
Affiliations
Review

[Protein ubiquitination on the regulation of inflammatory bowel disease]

[Article in Chinese]
Jing Ling et al. Zhejiang Da Xue Xue Bao Yi Xue Ban. .

Abstract
in English, Chinese

Inflammatory bowel disease refers to chronic inflammatory disorders that affect the gastrointestinal tract. Ubiquitination is an important protein post-translational modification. In recent years, the research of ubiquitination-deubiquitination system in the development of inflammatory bowel disease has become a hot spot. Up to now, the E3 ubiquitin ligases such as ring finger protein 183 (RNF183), RNF20, Itch and A20 were well studied in inflammatory bowel disease. RNF183 promotes the activation of the NF-κB pathway by increasing the ubiquitination and degradation of IκBα; RNF20 drives histone H2B monoubiquitylation, downregulates a panel of inflammation-associated genes; Itch inhibits IL-17-mediated colon inflammation by retinoid acid related orphan receptor γt ubiquitination; A20 has ubiquitinating-deubiquitinating activity to regulates colon inflammation. This article reviews the role and regulatory mechanism of RNF183, RNF20, Itch and A20 in the pathogenesis of inflammatory bowel disease.

炎性肠疾病是一种慢性胃肠道功能紊乱的炎症性疾病。泛素化是一类重要的蛋白质翻译后修饰方式。近年来关于泛素化-去泛素化系统在炎性肠疾病发生和发展中的作用已成为研究热点。目前蛋白泛素化修饰调控炎性肠疾病过程所需的E3泛素连接酶中，分子生物学研究较为清楚的有环指蛋白183（RNF183）、环指蛋白20（RNF20）、Itch和锌指蛋白A20。其中RNF183可靶向核因子κB抑制蛋白α（IκBα）泛素化降解促进NF-κB活化；RNF20促进组蛋白H2B单泛素化从而下调相关炎症因子的转录；Itch促进维甲酸核孤儿受体γt泛素化降解抑制IL-17介导的肠炎；A20以其特有的泛素化和去泛素化双重活性影响炎性肠疾病的发展。本文综述了以上分子在炎性肠疾病发生、发展和转归中的作用及调控机制。

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