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RAVER1 is a coactivator of MDA5-mediated cellular antiviral response Free
He Chen, Ying Li, Jing Zhang, Yong Ran, Jin Wei, Yan Yang, and Hong-Bing Shu*
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China *Correspondence to:Hong-Bing Shu, Tel: 86-27-68753795; Fax: 86-27-68753780; E-mail: shuh@whu.edu.cn
J Mol Cell Biol, Volume 5, Issue 2, April 2013, 111-119,  https://doi.org/10.1093/jmcb/mjt006
Keyword: MDA5, RAVER1, coactivator, signaling, innate immunity

Detection of viral nucleic acids by pattern recognition receptors initiates type I interferon (IFN) induction and innate antiviral response. The RIG-I-like receptors (RLRs), including RIG-I and MDA5, recognize cytoplasmic viral RNA in most cell types and are critically involved in innate antiviral response. RIG-I and MDA5 are structurally related and mediate similar signaling pathways. While the regulation of RIG-I activity has been extensively investigated, little is known about the regulatory mechanisms of MDA5 activity. Here we identified ribonucleoprotein PTB-binding 1 (RAVER1) as a specific MDA5-interacting protein. RAVER1 was associated with MDA5 upon viral infection. Overexpression of RAVER1 at low dosages enhanced MDA5- but not RIG-I-mediated activation of the IFN-β promoter, whereas knockdown of RAVER1 inhibited MDA5- but not RIG-I-mediated induction of downstream antiviral genes. Mechanistically, overexpression of RAVER1 enhanced the binding of MDA5 to its ligand poly(I:C), whereas knockdown of RAVER1 had opposite effect. Our findings suggest that RAVER1 specifically regulates MDA5 activity, revealing a mechanism of differential regulation of MDA5- and RIG-I-mediated innate antiviral response.