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The APC10 subunit of the anaphase-promoting complex/cyclosome orchestrates NLRP3 inflammasome activation during the cell cycle
FEBS Letters ( IF 3.5 ) Pub Date : 2021-08-18 , DOI: 10.1002/1873-3468.14181
Siyu Huang 1 , Pin Wan 2 , Shanyu Huang 1 , Siyu Liu 1 , Qi Xiang 1 , Ge Yang 1 , Muhammad Adnan Shereen 1 , Pan Pan 2 , Jun Wang 3 , Weiyong Liu 4 , Kailang Wu 1 , Jianguo Wu 1, 2, 5
Affiliation  

The activation of the NLRP3 inflammasome plays a crucial role in the innate immune response. During cell division, NLRP3 inflammasome activation must be strictly controlled. In this study, we discover that the anaphase-promoting complex subunit 10 (APC10), a substrate recognition protein of the anaphase-promoting complex/cyclosome (APC/C), is a critical mediator of NLRP3 inflammasome activation. During interphase, APC10 interacts with NLRP3 to promote NLRP3 inflammasome activation, whereas during mitosis, APC10 disassociates from the NLRP3 inflammasome to repress inflammatory responses. This study reveals a distinct mechanism by which APC10 serves as a switch for NLRP3 inflammasome activation during the cell cycle.

中文翻译:

后期促进复合物/环状体的 APC10 亚基在细胞周期中协调 NLRP3 炎症小体的激活

NLRP3 炎症小体的激活在先天免疫反应中起着至关重要的作用。在细胞分裂过程中,必须严格控制 NLRP3 炎症小体的激活。在这项研究中,我们发现后期促进复合物亚基 10 (APC10),一种后期促进复合物/环体 (APC/C) 的底物识别蛋白,是 NLRP3 炎症小体激活的关键介质。在间期,APC10 与 NLRP3 相互作用以促进 NLRP3 炎症小体激活,而在有丝分裂期间,APC10 与 NLRP3 炎症小体分离以抑制炎症反应。这项研究揭示了一种独特的机制,通过该机制,APC10 在细胞周期中充当 NLRP3 炎症小体激活的开关。
更新日期:2021-10-12
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