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Updated: Feb 3, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
TARBP2 negatively regulates IFN-β production and innate antiviral response by targeting MAVS
Ting Ling1, Sheng-Na Li1, Guang-Xiu Weng1
1Key Laboratory of Functional Small Organic Molecules, Ministry of Education and College of Life Science, Jiangxi Normal University, Nanchang, Jiangxi, 330022, China.
Abstract:
MAVS as an essential receptor protein for anti-virus innate immunity plays an important role in the production of virus-induced typeⅠ interferon and regulation of interferon regulatory factor 3/7. Understanding the MAVS-mediated antiviral signaling pathway can provide detailed insights. In this study, we identify transactivation response element RNA-binding protein (TARBP2), as an inhibitor of the cellular protein kinase PKR, negatively regulates virus -induced IFN-β production by targets MAVS. Overexpression of TARBP2 inhibits virus-induced IFN-β production as well as cellular antiviral response. Then knockdown of TARBP2 inhibited virus-induced IFN-β signaling. Further studies demonstrated that TARBP2 interacted with MAVS and targeted MAVS to abrogate MAVS-RIG-I and MAVS-TRAF3 association. Our findings suggest that TARBP2 is an important non-redundant virus-mediated negative regulator of typeⅠ interferon.
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