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. 2005 May 17;308(1):196–210. doi: 10.1016/j.yexcr.2005.04.016

Fig. 4.

Fig. 4

ICP0-mediated AP-1 activation is inhibited by c-Jun (S73A), c-Jun (S63/73A), but not by p38 (AF), ERK1 (K71R) and ERK2 (K52R). Activation of AP-1 by ICP0 is inhibited by c-Jun (S73A) (a) and c-Jun (S63/73A) (b). ICP0 and AP-1-Luc together with the internal control were transfected into 293T cells without or with his-c-Jun (S73A) (a) or his-c-Jun (S63/73A) (b). Cells were pelleted, lysed and assayed for relative luciferase activity 48 h after transfection. Lower panels: expression of the indicated constructs. (c) The dominant-negative mutant p38 (AF) significantly reduced UV-induced AP-1 activation, while it had no inhibitory effect on AP-1 activation by ICP0. Flag-p38 (AF), AP-1-Luc reporter gene and internal control were introduced into 293T cells together with ICP0 or LacZ respectively. 36 h post transfection, cells transfected with LacZ and reporter gene were exposed to UV irradiation. After 30 min of exposure and 30 more minutes of incubation, the irradiated and unirradiated cells were collected for dual-luciferase assay. Activation of AP-1 by ICP0 is not inhibited by ERK1 (K71R) (d) or attenuated by ERK2 (K52R) (e). Upper panel: AP-1-Luc activation by ICP0 in the presence of gradient amounts of ERK1 (K71R) or ERK2 (K52R). Lower panels: expression of the indicated constructs.