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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWInterferon regulatory factor 3 (IRF3) is a member of the IRF family. It plays a crucial role in activation of innate immunity and inflammation in response to viral infection, functioning as a molecular switch for antiviral activity.1,2,3,4,5 Double-stranded RNA generated during a viral infection leads to IRF3 activation by serine/threonine phosphorylation by TBK1 or IKBKE kinases, which induces a conformational change leading to its dimerization, nuclear localization, and association with CREBBP.1,2,3,6 The complex, known as DRAF1, activates transcription interferons alpha and beta, as well as other interferon-induced genes.1,6 These genes play a critical role in type 1 interferon (IFN)-dependent immune response.5 A recent study shows phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF recruits and specifies IRF3 phosphorylation and activation by the serine/threonine-protein kinase TBK1, thereby inducing the production of type-1 interferons.2,4,7
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1. Structural insights into the functions of TBK1 in innate antimicrobial immunity. Structure 21(7), 1137-1148 (2013).
2. SIKE is an IKKε/TBK1-
3. Recognition of the measles virus nucleocapsid as a mechanism of IRF-
4. VISA is an adapter protein required for virus-
5. The impact of the interferon/TNF-
6. Human DEAD box helicase 3 couples IκB kinase ε to interferon regulatory factor 3 activation. Mol. Cell. Biol. 33(10), 2004-2015 (2013).
7. Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation. Science 347(6227), aaa2630 (2015).