FIGURE 6.

ARL16 working model. A, endogenous ARL16 binds with GTP during infection. 293T cells (1 × 10⁶) were infected with SV or left untreated for 12 h before lysis. Cell lysates were immunoprecipitated with ARL16 antiserum. The immunoprecipitates were separated by SDS-PAGE, transferred to nitrocellulose filters and after renaturation allowed to bind [α-³²P]GTP as in Fig. 5C. B, in the absence of viral infection, ARL16 is in its GTP-disassociated and inactive state. With virus stimulation, it changes into the GTP binding active state and sequesters the CTD of RIG-I, finally inhibiting RIG-I-mediated downstream signaling events.