Danying Chen

Hong-Bing Shu

Jikun Zha

Ke-Jun Han

Liang-Guo Xu

Qianhe Zhou

Wei He

Zhonghe Zhai

Abstract
               IFN regulatory factor-3 is a transcription factor that is required for the rapid induction of type I IFNs in the innate antiviral response. Two noncanonical IκB kinase (IKK) family members, IKKε and TRAF family-associated NF-κB activator-binding kinase-1, have been shown to phosphorylate IFN regulatory factor-3 and are critically involved in virus-triggered and TLR3-mediated signaling leading to induction of type I IFNs. In yeast two-hybrid screens for potential IKKε-interacting proteins, we identified Ret finger protein (RFP) as an IKKε-interacting protein. Coimmunoprecipitation experiments indicated that RFP interacted with IKKε and TRAF family-associated NF-κB activator-binding kinase-1 as well as the two canonical IKK family members, IKKβ and IKKα. RFP inhibited activation of the IFN-stimulated response element and/or NF-κB mediated by the IKK family members and triggered by TNF, IL-1, polyinosinic-polycytidylic acid (ligand for TLR3), and viral infection. Moreover, knockdown of RFP expression by RNA interference-enhanced activation of IFN-stimulated response element and/or NF-κB triggered by polyinosinic-polycytidylic acid, TNF, and IL-1. Taken together, our findings suggest that RFP negatively regulates signaling involved in the antiviral response and inflammation by targeting the IKKs.</jats:p

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The Journal of Immunology

The Ret Finger Protein Inhibits Signaling Mediated by the Noncanonical and Canonical IκB Kinase Family Members

The Ret Finger Protein Inhibits Signaling Mediated by the Noncanonical and Canonical IκB Kinase Family Members

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