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. Author manuscript; available in PMC: 2011 Jul 25.
Published in final edited form as: Nat Struct Mol Biol. 2008 Nov 30;16(1):63–70. doi: 10.1038/nsmb.1529

Figure 5. Effects of PKR variants on sensitivity to pseudosubstrate inhibition in HeLa cells.

Figure 5

(a) Human HeLa PKRkd cells were co-transfected with expression vectors for luciferase, knock-down resistant derivatives of human (h)PKR, hPKR-E379R or hPKR-A488E and control, vacK3L, vacK3L-H47R or swpvC8L. After 40 hours, cells were harvested, lysed, and samples were assayed for luciferase activity. Luciferase activity was normalized to control transfections lacking PKR inhibitors. Standard deviations are indicated for three independent transfections. Significant differences are indicated: * = p<0.005; ** = p<0.001; n.s. = not significant (p > 0.05). (b) Co-transfection of luciferase, hPKR, hPKR-A488E, mouse (m)PKR or mPKR-E451A and vacK3L or swinepox C8L. (c) Immunoblot analyses of whole cell extracts from cells transfected with the indicated expression vectors in the absence (−) or presence (+) of vacK3L. The blots were probed with antiserum specific for phosphorylated Ser51 in eIF2α (upper panel), total human eIF2α (second panel), hPKR (third panel), or mPKR (bottom panel).