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2025 01 v.41 71-78
RNF126介导IKKγ的K63位泛素化促进EV71感染炎症反应的机制研究
基金项目(Foundation): 深圳市科创委基础研究面上项目(项目号:JCYJ20230807151802006),题目:HAUSP通过NLRP3/IL-1β调控EV71感染炎症反应的机制研究~~
邮箱(Email): mengjun079@163.com;
DOI: 10.13242/j.cnki.bingduxuebao.004628
中文作者单位:

南方医科大学公共卫生学院;深圳市疾病预防控制中心病原微生物检测所;

摘要(Abstract):

研究RNF126在EV71感染炎症反应调控中的作用及相关机制。在THP-1诱导分化的巨噬细胞中,以特异性靶向RNF126的干扰RNA降低RNF126表达作为干扰组,以阴性对照干扰RNA作为对照组,以EV71感染不同时间,采用实时荧光定量PCR和ELISA分别检测IL-6、TNF-α、CCL3的mRNA和蛋白质水平表达变化;通过实时荧光定量PCR检测EV71-VP1表达变化;采用空斑形成试验检测病毒滴度变化;以Western blot检测天然免疫NF-κB信号通路相关蛋白的磷酸化和表达变化。通过免疫共沉淀检测RNF126相互作用靶蛋白;观察RNF126对靶蛋白泛素化修饰的影响。结果发现,在EV71感染时,干扰RNF126表达后与对照组相比:IL-6、TNF-α和CCL3的mRNA和蛋白质水平表达显著减少(P<0.05),EV71-VP1表达增强(P<0.05),病毒滴度增高;NF-κB信号通路中IKKα/β、IκBα和p65磷酸化水平下降,IKKγ、IKKα及p65总蛋白表达无明显变化,IκBα表达增加。RNF126与IKKγ相互作用并介导其K63位泛素化活化。以上结果说明,EV71感染时,RNF126与IKKγ相互作用并介导其K63位泛素化,促进NF-κB信号通路活化及其下游细胞炎症因子产生,抑制病毒复制。

关键词(KeyWords): 肠道病毒71型;环指蛋白126;天然免疫;泛素化
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基本信息:

DOI:10.13242/j.cnki.bingduxuebao.004628

中图分类号:R373.2

引用信息:

[1]林小嫚,潘倩瑜,何雅青等.RNF126介导IKKγ的K63位泛素化促进EV71感染炎症反应的机制研究[J].病毒学报,2025,41(01):71-78.DOI:10.13242/j.cnki.bingduxuebao.004628.

基金信息:

深圳市科创委基础研究面上项目(项目号:JCYJ20230807151802006),题目:HAUSP通过NLRP3/IL-1β调控EV71感染炎症反应的机制研究~~

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