...
【24h】

Japanese flounder pol-miR-3p-2 suppresses Edwardsiella tarda infection by regulation of autophagy via p53

机译:日本比目鱼POL-MIR-3P-2通过P53调节自噬抑制Edwardsiella Tarda感染

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

MicroRNAs (miRNAs) are post-transcriptional regulators that play vital roles in diverse physiological processes including immunity. In this study, we investigated the regulatory mechanism and function of a novel Japanese flounder (Paralichthys olivaceus) miRNA, pol-miR-3p-2. pol-miR-3p-2 was responsive in expression to the infection of the bacterial pathogen Edwardsiella tarda. pol-miR-3p-2 negatively regulated the expression of p53 through interaction with the 3'UTR of p53. Overexpression of pol-miR-3p-2 promoted autophagy, resulting in augmented production of LC3-II, while knockdown of p53 increased the level of beclin, a key factor of autophagy. In vivo and in vitro studies showed that E. tarda infection induced autophagy in flounder, and pol-miR-3p-2 inhibited the infectivity of E. tarda. Together these results indicate that pol-miR-3p-2 regulates autophagy through the target gene p53, thus revealing a regulatory link between p53 and autophagy in teleost, and that pol-miR-3p-2 plays an important role in the immune defense against E. tarda.
机译:Micrornas(miRNA)是转录后调节因子,在不同的生理过程中起重要作用,包括免疫力。在这项研究中,我们调查了一种新型日本比目鱼(Paralichthys Olivaceus)miRNA,Pol-miR-3p-2的监管机制和功能。 Pol-miR-3p-2对表达对细菌病原体Edwardella Tarda感染的反应性。 POL-MIR-3P-2通过与P53的3'UTR相互作用来负调节P53的表达。 Pol-miR-3p-2的过度表达促进了自噬,导致LC3-II的增强生产,而P53的敲低增加了BECLIN的水平,是自噬的关键因素。体内和体外研究表明,E.TARDA感染诱导鼠甘卵中的自噬,POL-MIR-3P-2抑制E. TARDA的感染性。这些结果表明,POL-MIR-3P-2通过靶基因P53调节自噬,从而揭示了P53和Teactiophy的自噬之间的调节联系,并且Pol-MiR-3P-2在免疫防御中起着重要作用E. Tarda。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号