| First Author | Zhang HX | Year | 2013 |
| Journal | Proc Natl Acad Sci U S A | Volume | 110 |
| Issue | 16 | Pages | 6459-64 |
| PubMed ID | 23553835 | Mgi Jnum | J:196169 |
| Mgi Id | MGI:5486625 | Doi | 10.1073/pnas.1304432110 |
| Citation | Zhang HX, et al. (2013) Rig-I regulates NF-kappaB activity through binding to Nf-kappab1 3'-UTR mRNA. Proc Natl Acad Sci U S A 110(16):6459-64 |
| abstractText | 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-kappab1. Rig-I is required for NF-kappaB activity via regulating Nf-kappab1 expression at posttranscriptional levels. It interacts with the multiple binding sites within 3'-UTR of Nf-kappab1 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-kappab1 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-kappab1 and 3'-UTR-mediated luciferase expression levels. These findings indicate that Rig-I functions as a positive regulator for NF-kappaB signaling and is involved in multiple biological processes in addition to host antivirus immunity. |
