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. Author manuscript; available in PMC: 2015 Jun 19.
Published in final edited form as: Immunity. 2014 Jun 12;40(6):936–948. doi: 10.1016/j.immuni.2014.05.007

Fig. 3. OASL antiviral activity is dependent on RIG-I.

Fig. 3

(A–B) Loss of RIG-I expression reduces OASL antiviral activity against VSV. Cells were transfected with 50 nM RIG-I or control siRNA (Dharmacon) for 48 h, followed by VSV infection (1 m.o.i., 24 h). Total RNA from the infected cells were extracted and analyzed for VSV replication (A) and RIG-I mRNA (B) by qRT-PCR. (C) Indicated cells were transfected with psiRNA-Ctrl or psiRNA-hRIG-I plasmids (Invivogene) followed by Zeocin selection. VSV infected (1 m.o.i) cells were immunobloted with indicated antibodies. (D) Levels of RIG-I silencing were estimated by qRT-PCR. (E–F) Expression of OASL in RIG-I null cells does not protect them from VSV. OASL expressing 293T-DDX58−/− and control cells were infected with 1 m.o.i VSV for 24 h followed by IB with indicated antibodies (E), and qRT-PCR to detect VSV replication (F).