FIG. 5.

MEK2, but not MEK1, is responsible for interruption of IFN-induced antiviral responses. RNA oligonucleotides to MEK1 (MEK1RNAi), MEK2 (MEK2RNAi), or random sequence (NGRNAi) were transfected to RasV12 cells twice with a 24-h interval. At 24 h after the second RNAi treatment, the cells were incubated with IFN (500 U/ml) for 16 h followed by infection of VSV (MOI = 1). (A) Knockdown of MEK1 and MEK2 mRNA expression by RNAi. Total cellular RNA was extracted at 24 h after the RNAi treatment and subjected to RT-PCR for MEK1, MEK2, and GAPDH. (B) Viral protein synthesis in vector control cells (Cont) and RasV12 cells (V12) with RNAi-mediated depletion of MEK1 or MEK2 at 24 h after VSV infection as determined by Western blot analysis for VSV-G, phosphorylated ERK (p-ERK), and total ERK-1/2 (t-ERK) at 24 h after VSV infection.