生物
夏普
泛素连接酶
节点1
泛素
细胞生物学
凋亡抑制因子
先天免疫系统
免疫系统
模式识别受体
受体
信号转导
炎症
节点2
癌症研究
免疫学
半胱氨酸蛋白酶
生物化学
细胞凋亡
程序性细胞死亡
基因
作者
Joseph Topal,Mads Gyrd‐Hansen
标识
DOI:10.1016/j.semcdb.2020.07.001
摘要
The receptor-interacting protein kinases (RIPKs) are key regulators of inflammatory signalling and cell death pathways triggered by innate immune receptors, and RIPKs have emerged as promising therapeutic targets for treatment of immune-related disorders. RIPK2 mediates signalling responses initiated by the bacterial-sensing pattern recognition receptors nucleotide-binding oligomerization domain-containing proteins 1 and 2 (NOD1/2), which play a key role in regulation of intestinal immunity and inflammation. Modification of RIPK2 by non-degradative ubiquitin chains generated by the E3 ubiquitin ligase XIAP and other ligases govern NOD1/2 signalling. Recent advances suggest that the interaction between RIPK2 and XIAP is a druggable protein-protein interaction to modulate NOD1/2-dependent immune responses. Here, we discuss the mechanistic function of RIPK2 in immune signalling, its clinical relevance, and the on-going efforts to target RIPK2 in inflammatory bowel disease and beyond.
科研通智能强力驱动
Strongly Powered by AbleSci AI