| First Author | Jiang C | Year | 2016 |
| Journal | Cell Rep | Volume | 14 |
| Issue | 10 | Pages | 2389-401 |
| PubMed ID | 26947079 | Mgi Jnum | J:234562 |
| Mgi Id | MGI:5790270 | Doi | 10.1016/j.celrep.2016.02.031 |
| Citation | Jiang C, et al. (2016) CARMA3 Is a Host Factor Regulating the Balance of Inflammatory and Antiviral Responses against Viral Infection. Cell Rep 14(10):2389-401 |
| abstractText | Host response to RNA virus infection is sensed by RNA sensors such as RIG-I, which induces MAVS-mediated NF-kappaB and IRF3 activation to promote inflammatory and antiviral responses, respectively. Here, we have found that CARMA3, a scaffold protein previously shown to mediate NF-kappaB activation induced by GPCR and EGFR, positively regulates MAVS-induced NF-kappaB activation. However, our data suggest that CARMA3 sequesters MAVS from forming high-molecular-weight aggregates, thereby suppressing TBK1/IRF3 activation. Interestingly, following NF-kappaB activation upon virus infection, CARMA3 is targeted for proteasome-dependent degradation, which releases MAVS to activate IRF3. When challenged with vesicular stomatitis virus or influenza A virus, CARMA3-deficient mice showed reduced disease symptoms compared to those of wild-type mice as a result of less inflammation and a stronger ability to clear infected virus. Altogether, our results reveal the role of CARMA3 in regulating the balance of host antiviral and pro-inflammatory responses against RNA virus infection. |
