USP5通过稳定TXNIP蛋白来促进脂多糖诱导的亡和炎症反应
Songchang Shi1, Xiaobin Pan1, Minyong Chen2
1Department of Critical Care Medicine, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital South Branch, Fujian Provincial Hospital, Fuzhou, Fujian Province, China.
Hepatology communications
|August 3, 2023
概括
乌比基特异性蛋白酶5 (USP5) 稳定了铁素相互作用蛋白 (TXNIP),促进了肝脏炎症和亡. USP5 TXNIP的二双化驱动了脂聚糖诱导的肝损伤.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 脂聚糖 (LPS) 诱导的肝损伤机制尚未完全理解.
- 在这个过程中,硫素相互作用蛋白 (TXNIP) 的作用需要进一步阐明.
研究的目的:
- 调查二维基基因酶在调节TXNIP稳定性的作用.
- 为了探索二维基丁酶-TXNIP相互作用对肝细胞炎症的影响.
主要方法:
- 通过过度表达和共免疫沉来调节TXNIP水平的杜比基因酶的查.
- 使用细胞模型 (Huh7,HepG2) 与二维基丁酶倒置和TXNIP过度表达.
- 用脂多糖诱导炎症以评估细胞反应.
主要成果:
- 鉴定出乌比基特异性蛋白酶5 (USP5) 通过duebiquitylation与TXNIP相互作用和稳定.
- 在LPS治疗的细胞中USP5的敲击降低了细胞亡和炎症标志物 (NLRP3,IL-1β,IL-18,ASC,procaspase-1).
- 过度表达TXNIP逆转了USP5淘汰后观察到的保护作用.
结论:
- 通过稳定TXNIP,USP5促进LPS诱导的肝细胞亡和炎症.
- 通过USP5调节的TXNIP稳定是肝炎反应的关键机制.
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