Journal Article

Rig-I regulates NF-?B activity through binding to Nf-kappab1 3'-UTR mRNA

Kuang, Ying, Li, Yi-Xue, Chen, Zhu, Dang, Su-Ying, Zheng, Guang-Yong, Sun, Yue-Ping, Zhu, Hou-Bao, Wang, Zhu-Gang, Zhang, Hong-Xin, Liu, Xue-Song, Liu, Zi-Xing, Zhu, Jiang, Lu, Shun-Yuan, Huang, Qiu-Hua, Chen, Sai-Juan, Xie, Yin-Yin, Fei, Jian, Chen, Hai-Feng

2013

Overview

Retinoic acid inducible gene I (RIG-I) senses viral RNAs and triggers innate antiviral responses through induction of type I IFNs and inflammatory cytokines. However, whether RIG-I interacts with host cellular RNA remains undetermined. Here we report that Rig-I interacts with multiple cellular mRNAs, especially Nf-Kb1. Rig-I is required for NF-KB activity via regulating Nf-Kb1 expression at posttranscriptional levels. It interacts with the multiple binding sites within 3'-UTR of Nf-Kb1 mRNA. Further analyses reveal that three distinct tandem motifs enriched in the 3'-UTR fragments can be recognized by Rig-I. The 3'-UTR binding with Rig-I plays a critical role in normal translation of Nf-Kb1 by recruiting the ribosomal proteins [ribosomal protein L13 (Rpl13) and Rpl8] and rRNAs (18S and 28S). Down-regulation of Rig-I or Rpl13 significantly reduces Nf-Kb1 and 3'-UTR-mediated luciferase expression levels. These findings indicate that Rig-I functions as a positive regulator for NF-KB signaling and is involved in multiple biological processes in addition to host antivirus immunity. [PUBLICATION ABSTRACT]

• Publisher: National Academy of Sciences
• Subject: Binding sites / Cytokines / Gene expression / Ribonucleic acid / RNA / Signal transduction