MicroRNAs （miRNAs） recruit the RNA-induced silencing complex （RISC） to repress the translation of target mRNAs. While the 5＇ 7-methylguanosine cap of target mRNAs has been well known to be important for miRNA rep...MicroRNAs （miRNAs） recruit the RNA-induced silencing complex （RISC） to repress the translation of target mRNAs. While the 5＇ 7-methylguanosine cap of target mRNAs has been well known to be important for miRNA repression, the underlying mechanism is not clear. Here we show that TNRC6A interacts with elF4E2, a homo- Iogue of eIF4E that can bind to the cap but cannot interact with eIF4G to initiate translation, to inhibit the translation of target mRNAs. Downregulation of eIF4E2 relieved miRNA repression of reporter expression. Moreover, eIF4E2 downregulation increased the protein levels of endogenous IMP1, PTEN and PDCD4, whose expression are repressed by endogenous miRNAs. We further provide evidence showing that miRNA enhances elF4E2 association with the target mRNA. We propose that miRNAs recruit eI4E2 to compete with eIF4E to repress mRNA translation.展开更多
文摘目的观察肾移植大鼠外周血中CD4+CD25+调节性T细胞及其表面标志物Foxp3、ABCC4、e IF6基因表达,结合白细胞介素-2(IL-2)和肿瘤坏死因子-γ(INF-γ)水平及肝、肾功能变化进行相关分析,探讨其在移植免疫排斥机制中的作用及意义。方法监测急排组与非急排组大鼠肝、肾功能;ELISA方法检测血浆中IL-2和INF-γ的表达水平;流式细胞仪检测CD4+、CD8+、CD4+CD25+Treg细胞亚群;荧光PCR检测CD4+CD25+Treg细胞Foxp3、ABCC4及e IF6 m RNA表达。结果与术前相比,急排组术后第7天血清肌酐、尿素氮均明显升高(P<0.05);急排组术后第7天IL-2及IFN-γ均升高,差异有统计学意义(P<0.05);急排组术后CD3+、CD4+、CD8+水平明显升高,差异有统计学意义(P<0.05);与非急排组相比,急排组术后CD4+CD25+Treg细胞表达降低,差异有统计学意义(P<0.05)。与非急排组相比,急排组术后Foxp3+基因表达量明显降低,ABCC4、e IF6基因表达量升高,差异有统计学意义(P<0.05)。结论 CD4+CD25+调节性T细胞在肾移植排斥反应中起到重要作用,CD4+CD25+Treg细胞Foxp3、ABCC4及e IF6 m RNA参与急性排斥反应的发生,检测其变化可辅助诊断急性排斥反应的发生。
文摘MicroRNAs （miRNAs） recruit the RNA-induced silencing complex （RISC） to repress the translation of target mRNAs. While the 5＇ 7-methylguanosine cap of target mRNAs has been well known to be important for miRNA repression, the underlying mechanism is not clear. Here we show that TNRC6A interacts with elF4E2, a homo- Iogue of eIF4E that can bind to the cap but cannot interact with eIF4G to initiate translation, to inhibit the translation of target mRNAs. Downregulation of eIF4E2 relieved miRNA repression of reporter expression. Moreover, eIF4E2 downregulation increased the protein levels of endogenous IMP1, PTEN and PDCD4, whose expression are repressed by endogenous miRNAs. We further provide evidence showing that miRNA enhances elF4E2 association with the target mRNA. We propose that miRNAs recruit eI4E2 to compete with eIF4E to repress mRNA translation.
