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. 2003 Apr;77(7):4315–4325. doi: 10.1128/JVI.77.7.4315-4325.2003

FIG. 2.

FIG. 2.

ICP27 is required for CK2 activation. (A) Equal amounts of mock-infected cell extracts (lane 2) or cell extracts infected with different mutant viruses were subjected to the casein-containing in situ kinase assay as follows: lane 1, wt KOS; lane 3, dl1403; lane 4, 27LacZ; lane 5, in1814; and lane 6, tk−. (B) Equal amounts of cell extracts infected with the wt or with mutants with different mutations in the ICP27 gene and collected at 6 h postinfection were subjected to the in situ gel kinase assay. Infection with tsR480H at the permissive temperature (32°C) activated CK2 (lane 3), but infection at the restrictive temperature (39.2°C; lane 4), at which ICP27 is deficient in nucleocytoplasmic shuttling, did not. Infection with the M15 (lane 2) or the d1-2 (lane 6) deletion mutant, both of which also disrupt ICP27 shuttling, failed to activate the CK2 α′ subunit. The ICP27 viral mutants vBS3.3 (lane 5), vBSL387N (lane 7), d2-3 (lane 8), and d5-6 (lane 9) activate CK2 to levels similar to that activated by the wt (lane 1).