Interferons (IFN)s are involved in a multitude of immune interactions during viral infections and play a major role in both the induction and regulation of innate and adaptive antiviral mechanisms (1 for review). During infection, host-virus interactions signal downstream molecules such as transcription factors such as IFN regulatory factor-3 (IRF3) which can act to stimulate transcription of IFN-alpha/beta genes. IRF3 is present in an inactive form in the cytoplasm of most cells (2). Following viral infection, IRF3 can be activated by IkappaB kinase-epsilon and TANK-binding kinase 1 (TBK1) (3,4), whereupon IRF3 translocates to the nucleus. IRF3 can also be activated by stimulation of toll-like receptor 3 (TLR3) by dsRNA (3,5). IRF3 exists as at least two distinct isoforms.
Toll-like receptor signaling pathway
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