FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1

Jae Hoon Kim, Min Eun Park, Chamilani Nikapitiya, Tae Hwan Kim, Md Bashir Uddin, Hyun Cheol Lee, Eunhee Kim, Jin Yeul Ma, Jae U. Jung, Chul Joong Kim, Jong Soo Lee

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gtmice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.

Original languageEnglish (US)
Article numbere1006398
JournalPLoS pathogens
Volume13
Issue number5
DOIs
StatePublished - May 2017
Externally publishedYes

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Molecular Biology
  • Genetics
  • Virology

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