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CARMA3 Is a Host Factor Regulating the Balance of Inflammatory and Antiviral Responses against Viral Infection.


ABSTRACT: Host response to RNA virus infection is sensed by RNA sensors such as RIG-I, which induces MAVS-mediated NF-?B and IRF3 activation to promote inflammatory and antiviral responses, respectively. Here, we have found that CARMA3, a scaffold protein previously shown to mediate NF-?B activation induced by GPCR and EGFR, positively regulates MAVS-induced NF-?B activation. However, our data suggest that CARMA3 sequesters MAVS from forming high-molecular-weight aggregates, thereby suppressing TBK1/IRF3 activation. Interestingly, following NF-?B 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.

SUBMITTER: Jiang C 

PROVIDER: S-EPMC5842788 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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CARMA3 Is a Host Factor Regulating the Balance of Inflammatory and Antiviral Responses against Viral Infection.

Jiang Changying C   Zhou Zhicheng Z   Quan Yanping Y   Zhang Shilei S   Wang Tingting T   Zhao Xueqiang X   Morrison Clayton C   Heise Mark T MT   He Wenqian W   Miller Matthew S MS   Lin Xin X  

Cell reports 20160303 10


Host response to RNA virus infection is sensed by RNA sensors such as RIG-I, which induces MAVS-mediated NF-κB and IRF3 activation to promote inflammatory and antiviral responses, respectively. Here, we have found that CARMA3, a scaffold protein previously shown to mediate NF-κB activation induced by GPCR and EGFR, positively regulates MAVS-induced NF-κB activation. However, our data suggest that CARMA3 sequesters MAVS from forming high-molecular-weight aggregates, thereby suppressing TBK1/IRF3  ...[more]

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