Fig. 14. The effect of other inducing agents that stimulate Activator Protein-1 (  AP-1 ) DNA binding activity. Exposure of CD3  +T cells to CD3/CD28-beads, tumor necrosis factor α, and serum induced AP-1 DNA binding activity (lanes 2, 4, 6, and 8). Sevoflurane inhibited CD3/CD28-induced (lane 5) and slightly tumor necrosis factor-induced (lane 7) AP-1 activity. In contrast, serum-induced AP-1 activation could not be inhibited by sevoflurane (lane 9). Equal amounts of protein from cell extracts were analyzed for AP-1 activity by electrophoretic mobility shift assay. ◂= position of AP-1 DNA complexes; ○= a nonspecific activity binding to the probe; ◃= unbound oligonucleotide. The data shown are representative of three independent experiments. 

Fig. 14. The effect of other inducing agents that stimulate Activator Protein-1 (  AP-1 ) DNA binding activity. Exposure of CD3  +T cells to CD3/CD28-beads, tumor necrosis factor α, and serum induced AP-1 DNA binding activity (lanes 2, 4, 6, and 8). Sevoflurane inhibited CD3/CD28-induced (lane 5) and slightly tumor necrosis factor-induced (lane 7) AP-1 activity. In contrast, serum-induced AP-1 activation could not be inhibited by sevoflurane (lane 9). Equal amounts of protein from cell extracts were analyzed for AP-1 activity by electrophoretic mobility shift assay. ◂= position of AP-1 DNA complexes; ○= a nonspecific activity binding to the probe; ◃= unbound oligonucleotide. The data shown are representative of three independent experiments. 

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