Fig 1.

ADAR1 deficiency enhances PKR activation following infection with WT, V^ko, or C^ko MV. (A) CON^kd, PKR^kd, and ADAR1^kd cells were either left uninfected (UI) or infected with WT, V^ko, or C^ko MV as indicated. At 24 h postinfection, whole-cell extracts were prepared and analyzed by Western immunoblot assay with antibodies against ADAR1, PKR, phospho-Thr446-PKR, MV H, GFP, and α-tubulin. XRP marks the position of ADAR1 antibody-cross-reacting protein (mobility slower than that of p150); the arrowhead marks the postulated caspase-mediated p120 ADAR1 cleavage product. (B) Quantification of n-fold activation of PKR, as measured by the level of phospho-Thr446-PKR to total PKR, determined by Western immunoblot analysis as shown in panel A. *, P < 0.05 by Student t test for comparison of PKR activation in uninfected cells and cells infected with WT, V^ko, or C^ko MV. The results shown are the means and standard errors of three independent experiments.