FIG 5.

The NOD of NLRX1 is crucial for mediating MAVS degradation. (A) Schematic illustration of MAVS truncations. (B) NLRX1 induces MAVS DII degradation. HLCZ01 cells were cotransfected with the V5-NLRX1 plasmid (1 μg) and the plasmids encoding the indicated domains of MAVS (1 μg) for 48 h. Cell lysates were analyzed by immunoblotting with the indicated antibodies. β-Actin was used as the loading control. FL, full length. (C) Schematic illustration of NLRX1 truncations. (D) The NLRX1 NOD promotes MAVS degradation. HLCZ01 cells were transfected with plasmids encoding the indicated domains of NLRX1 (2 μg) for 24 h and then inoculated with HCV (MOI of 0.1) for another 24 h, followed by immunoblotting with the indicated antibodies. β-Actin was used as the loading control. (E) The NLRX1 NOD inhibits HCV-induced IFN-β production. HLCZ01 cells were infected with HCV (MOI of 0.1) for 72 h, followed by transfection of the plasmids encoding the indicated domains of NLRX1 (2 μg) for 48 h. The induction of IFN-β was analyzed by real-time PCR and normalized to the value for GAPDH. Data are represented as means ± SD from triplicate experiments. *, P < 0.05.