Overexpression of wild-type 3C, the R84Q mutant (defective in RNA binding) of 3C, and EV-A71 infection (lanes 2, 6, and 8, Figure 4B) induced PKR phosphorylation, whereas this capacity was lost in the 3C catalytic-site mutants H40D, C147S, and H40D/C147S (lanes 3, 4, and 5, Figure 4B). Here, EIF2AK2 is linked to infection.