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

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.
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