文章摘要

头帕肿瘤综合征蛋白与肿瘤坏死因子受体介导的坏死样凋亡

作者: 1田静, 2王玉霞, 1彭军
1 中南大学药学院药理学系，长沙 410078
2 常德职业技术学院药学系，湖南 常德 415000
通讯: 彭军 Email: junpeng@csu.edu.cn
DOI: 10.3978/j.issn.2095-6959.2016.04.025
基金: 国家自然科学基金项目资助, 91439104; 81373409

摘要

头帕肿瘤综合征蛋白(cylindromatosis，CYLD)是一种去泛素化酶，其C-末端USP结构域具有催化功能，可移除受体相互作用蛋白激酶1(receptor interacting protein kinase 1，RIPK1)的K63连接泛素链，调节RIPK1的泛素化水平，从而参与调节肿瘤坏死因子受体1(tumor necrosis factor receptor 1，TNFR1)介导的RIPK依赖的细胞坏死样凋亡等病理生理过程。阐明CYLD对RIPK1去泛素化调节的详细机制，寻找针对CYLD的特异性抑制剂，可为与坏死样凋亡相关的损伤与疾病提供治疗的新策略。
关键词： CYLD 去泛素化 坏死样凋亡 受体相互作用蛋白激酶 肿瘤坏死因子受体1

CYLD and tumor necrosis factor receptor-mediated necroptosis

Authors: 1TIAN Jing, 2WANG Yuxia, 1PENG Jun
1 Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078
2 Department of Pharmacy, Changde Vocational Technical College, Changde Hunan 415000, China

CorrespondingAuthor: PENG Jun Email: junpeng@csu.edu.cn

DOI: 10.3978/j.issn.2095-6959.2016.04.025

Abstract

Cylindromatosis (CYLD) is a deubiquitinase, which regulates the level of ubiquitination for receptor interacting protein kinase 1 (RIPK1) by removing lysine 63-linked polyubiquitin chains. CYLD involves in the regulation of RIPK-dependent and tumor necrosis factor receptor 1 (TNFR1)-mediated cell necroptosis and other physiological and pathological processes. Clarification of the detailed mechanism of CYLD on RIPK1 and identification of specific inhibitor of this process will provide a new strategy for the treatment of the diseases associated with necroptosis.

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