Apr 14, 2011 · 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...

Mar 16, 2018 · We identified both common and dimer-specific DNA binding sites, and show that DNA-binding differences can translate into dimer-specific gene regulation. Central to the antiviral response, IRF3/5/7 regulate type I interferon (IFN) genes.

We show that IRF3 and IRF7 bind to many interferon-stimulated response element (ISRE)-type sites in the virus-response elements (VREs) of IFN promoters. However, strikingly, IRF5 does not bind the VREs, suggesting evolutionary selection against IRF5 homodimer binding.

The phosphatase protein phosphatase (PPP)1 can target four key phosphorylation sites (Ser471, -472, -477 and -479) of IRF7, attenuate the phosphorylation level and DNA-binding activity stimulated by IKKϵ, and inhibit IRF7-mediated IFN-I immune responses .

It has been shown that IRF7 can be activated by phosphorylation through TBK1/IKKϵ and TRIF-dependent pathways downstream of the cytoplasmic RNA/DNA sensor, and subsequently enters the nucleus, dimerizes with IRF3, exerts transcriptional activation and induces IFN-α/β expression .

IRF7 encodes interferon regulatory factor 7, a member of the interferon regulatory transcription factor (IRF) family. IRF7 has been shown to play a role in the transcriptional activation of virus-inducible cellular genes , including the type I interferon genes.

These studies demonstrate the regulation of IRF7 activity by phosphorylation-dependent allosteric changes that result in dimerization and that facilitate nuclear retention, derepress transactivation, and allow specific DNA binding.

May 19, 2011 · To characterize the conformational changes that occur on DNA binding and how they differ between IRF family members, we have solved the X-ray structures of IRF-3 and IRF-7 DBDs in the absence of DNA.

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

IRF-7 Is a Critical Regulator of Type 2 Innate Lymphoid Cells in Allergic Airway Inflammation. A Quantitative Genetic Interaction Map of HIV Infection. These findings provide further support for the essential role of IRF7 in amplifying antiviral IFN responses to ensure potent and sustained IFN responses during influenza virus infection in humans.