First Author | Kim JH | Year | 2017 |
Journal | PLoS Pathog | Volume | 13 |
Issue | 5 | Pages | e1006398 |
PubMed ID | 28542569 | Mgi Jnum | J:245551 |
Mgi Id | MGI:5916103 | Doi | 10.1371/journal.ppat.1006398 |
Citation | Kim JH, et al. (2017) FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1. PLoS Pathog 13(5):e1006398 |
abstractText | FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-kappaB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, 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. |