IRF7 Rabbit Recombinant mAb detects endogenous levels of total IRF7.

IRF7 is a multifunctional transcription factor originally identified in the context of Epstein-Barr virus (EBV) infection, and has since emerged as the crucial regulator of type I interferons (IFNs) against pathogenic infections, which activate IRF7 by triggering signaling cascades from pathogen recognition receptors (PRRs) that recognize pathogenic nucleic acids. Activation of IRF7 is prerequisite for its functions as a transcription factor. Inactive IRF7 resides in the cytoplasm as a "latent" form. Pathogenic infection triggers IRF7 phosphorylation and translocation into the nucleus, where with other co-activators it forms a transcriptional complex that binds to the promoter regions of target genes to activate transcription. IRF7 is activated by pathogenic nuclei acids through pathways mediated by TLR3, −7 and −9, RIG-I and likely DNA-dependent activator of IRF and IFI16, as well as by TLR2-mediated signaling pathway. It is a lymphoid-specific factor, which is constitutively expressed in the cytoplasm in B cells, pDCs and monocytes in the spleen, thymus, and peripheral blood lymphocytes, and is potently inducible by type I IFNs, virus infection and other stimuli such as 12-o-tetradecanoylphonol-13-acetate, TNFα and lipopolysaccharide in various cell types. IRF7 remains at low levels in most cell types, and has a very short half-life of 0.5-1 h in infected cells and approximately 5 h in uninfected cells but can be stabilized by the 26S proteasome inhibitor, MG132, or by a dominant-negative mutant of Cul1, a component of the SKP1-CUL1-F-box E3 ubiquitin ligase complex, suggesting that its stability is controlled by the ubiquitin–proteasome system. IRF7 can be regulated by various posttranslational modifications, including phosphorylation, ubiquitination, sumoylation and acetylation. It functions as the "master" regulator of type I IFN production, to be involved in the regulation of oncogenesis and apoptosis, implicated in autoimmune diseases and so on.