Rubicon modulates antiviral type I interferon (IFN) signaling by targeting IFN regulatory factor 3 dimerization

Jae Hoon Kim, Tae Hwan Kim, Hyun Cheol Lee, Chamilani Nikapitiya, Md Bashir Uddin, Min Eun Park, Prabuddha Pathinayake, Eun Seo Lee, Kiramage Chathuranga, Thilina U.B. Herath, W. A.Gayan Chathuranga, Jong Soo Lee

Research output: Contribution to journalArticlepeer-review


Rubicon is part of a Beclin-1-Vps34-containing autophagy complex. Rubicon induces antimicrobial responses upon Toll-like receptor (TLR) stimulation and functions as a feedback inhibitor to prevent unbalanced proinflammatory responses depending on dectin-1 signaling. However, the role played by Rubicon during antiviral immune responses, particularly the type I interferon (IFN) responses, remains largely unknown. Here, we report that Rubicon acts as a negative regulator for virustriggered IFN signaling. Knockdown of Rubicon promoted type I interferon signaling and inhibited virus replication, while overexpression of Rubicon had the opposite effect. Rubicon specifically interacts with the interferon regulatory factor (IRF) association domain (IAD) of IRF3, and this interaction leads to inhibition of the dimerization of IRF3, which negatively regulates IFN-mediated antiviral response. Thus, our findings suggest the novel additional role of Rubicon as a negative regulator that inhibits the IFN signaling and cellular antiviral responses, providing a novel cellular mechanism of IRF3 inhibition.

Original languageEnglish (US)
Article numbere00248-17
JournalJournal of virology
Issue number14
StatePublished - Jul 1 2017
Externally publishedYes


  • IRF3 dimerization
  • Interferon
  • Rubicon

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology


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