《Table 1 IRF3 regulators during virus infection》

  提示：宽带有限、当前游客访问压缩模式

本系列图表出处文件名：随高清版一同展现

《Balancing anti-viral innate immunity and immune homeostasis》

1. 获取 高清版本忘记账户？点击这里登录

1. 下载图表忘记账户？点击这里登录

Recent years have witnessed such modes of regulation；for example，miR-NAs have emerged as one of the key players to regulate gene expression by targeting the 3′-untranslated regions（UTR）of mRNA，resulting in degradation via cleavage，translational repression and deadenylation.7Similarly，phosphorylation and ubiquitination are wellcharacterized post-translational modifications that also control the intensity of the immune responses.Moreover，the anti-viral innate immune system is equipped with several molecules to down-regulatethe innate anti-viral response.The downregulation may be caused by direct interactions or posttranslational modifications，such as peptidyl-prolyl isomerase PIN1，FoxO1and TRIM21，which dampen the activation of IRF3（Table 1）.8–16Given the vital roles of IRF3 in the expression of an anti-viral state，via the production of pro-inflammatory molecules and type I and III IFNs，research is now focused primarily on identifying novel regulators（positive and negative），with the aim of finding new therapeutic targets during viral infection and combatting several autoimmune diseases.5