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RAVER1 is a coactivator of MDA5-mediated cellular antiviral response.

J Mol Cell Biol. 2013 Apr;5(2):111-9. Epub 2013 Feb 05
He Chen 1 , Ying Li , Jing Zhang , Yong Ran , Jin Wei , Yan Yang , Hong-Bing Shu
He Chen 1 , Ying Li , Jing Zhang , Yong Ran , Jin Wei , Yan Yang , Hong-Bing Shu
+ et al

[No authors listed]

Author information
  • 1 State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.

摘要


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.