IRF3 and viral infectious disease: The results revealed that overexpression of DYRK4 stabilized the exogenous or endogenous IRF3 protein (Fig. 5A,B), and under conditions of viral infection, overexpression of DYRK4 extended the half-life of the exogenous IRF3 protein (Fig. 5C) but did not affect IRF3 transcription (Fig. 5D).