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. 2010 Jul 29;6(7):e1001001. doi: 10.1371/journal.ppat.1001001

Figure 3. γHV68 infection activates IKKβ in a MAVS-dependent manner.

Figure 3

(A) Wild-type MEFs were treated with the IKKβ inhibitor, Bay11-7082, for 30 min at 0.5 h before infection or 7 h post-infection (h.p.i.) with γHV68. Cells were washed with medium and incubated for plaque formation. Plaques formed at 6 d.p.i. were counted. Data represent the mean ± SEM. (B) MEFs were infected with γHV68 (MOI = 10) and whole cell lysates of MEFs at indicated time points after γHV68 infection were precipitated with anti-IKKβ antibody. One half of IKKβ was used for an in vitro kinase assay with GST-IκBNT (amino terminal 50 amino acids of IκBα) (top) or analyzed by immunoblot (middle). Relative intensity of phosphorylated GST-IκBNT was normalized to IKKβ protein (bottom). (C) γHV68 infection was carried out as in (B) and whole cell lysates were analyzed by immunoblot with anti-IκBα (top) and β-actin (bottom). (D and E) Equal amount of live (MOI = 10) or UV-inactivated (UV) γHV68 was used to infect wild-type MEFs. The IKKβ kinase activity was assessed as in (B) and whole cell lysates were analyzed by immunoblot as in (C) for IκBα and β-actin. Graphs at the bottom show normalized IKKβ kinase activity (D) and IκBα protein (E).