Anti-IRF3 Antibody (N-Term)

Key transcriptional regulator of type I interferon (IFN) -dependent immune responses which plays a critical role in the innate immune response against DNA and RNA viruses. Regulates the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) in their promoters. Acts as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical role in both the early and late phases of the IFNA/B gene induction. Found in an inactive form in the cytoplasm of uninfected cells and following viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is phosphorylated by IKBKE and TBK1 kinases. This induces a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages.

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Cytoplasm. Nucleus Mitochondrion. Note=Shuttles between cytoplasmic and nuclear compartments, with export being the prevailing effect (PubMed:10805757, PubMed:35922005) . When activated, IRF3 interaction with CREBBP prevents its export to the cytoplasm (PubMed:10805757) . Recruited to mitochondria via TOMM70:HSP90AA1 upon Sendai virus infection (PubMed:25609812) .