Abstract
Genotoxic stress triggers signal transduction pathways that mediate either the protection or apoptosis of affected cells. The interferon regulatory factors (IRFs) are involved in a wide range of host defense mechanisms against environmental stresses. Treatment with DNA-damaging agents, including doxorubicin and UV radiation, caused phosphorylation of the IRF3 transcription factor. Phosphorylation of IRF3 induced its interaction with the transcriptional co-activator cAMP-response element binding protein-binding protein. Furthermore, genotoxic stress-induced phosphorylation of IRF3 resulted in its movement from the cytoplasm to the nucleus, where it activated transcription from its binding site. These observations suggest that IRF3 plays a role in the defensive responses induced by genotoxic stress.
Highlights
Genotoxic stress triggers signal transduction pathways that mediate either the protection or apoptosis of affected cells
IRF3-dependent gene expression was stimulated by viral infection but not by interferon ␥ treatment
The transcriptional activity of GAL4-IRF3 was strongly stimulated by UV radiation, which is known to cause genotoxic stress
Summary
Genotoxic stress triggers signal transduction pathways that mediate either the protection or apoptosis of affected cells. CAT activities were normalized to protein concentrations of cell extracts because the CMV promoter includes elements that are known to be inducible in response to genotoxic stress (24 –27). To identify agents that directly induce IRF3, we fused the IRF3 coding region to the DNA binding domain of GAL4 and examined the transcriptional activity of the GAL4-IRF3 fusion protein with a reporter plasmid containing GAL4 binding sites (Fig. 1A).
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