Abstract
Interferon regulatory factor 9 (IRF9) is an integral transcription factor in mediating the type I interferon antiviral response, as part of the interferon-stimulated gene factor 3. However, the role of IRF9 in many important non-communicable diseases has just begun to emerge. The duality of IRF9’s role in conferring protection but at the same time exacerbates diseases is certainly puzzling. The regulation of IRF9 during these conditions is not well understood. The high homology of IRF9 DNA-binding domain to other IRFs, as well as the recently resolved IRF9 IRF-associated domain structure can provide the necessary insights for progressive inroads on understanding the regulatory mechanism of IRF9. This review sought to outline the structural basis of IRF9 that guides its regulation and interaction in antiviral immunity and other diseases.
Highlights
Interferon regulatory factor 9 (IRF9) was first discovered as part of a protein subunit purified from the interferon-stimulated gene factor 3 (ISGF3) complex [1]
IRF9 is involved in regulating cell proliferation [4], tumor formation [7], cardiovascular disease [8], inflammation [9], autoimmune disease [10], and immune cell regulation [11], some of which is not related to ISGF3 complex
Interferon regulatory factor 9 was initially discovered as a component of the potent transcription factor ISGF3 responsible in initiating transcription of hundreds of interferon-stimulated genes (ISGs) to mount antiviral response
Summary
Interferon regulatory factor 9 (IRF9) was first discovered as part of a protein subunit purified from the interferon-stimulated gene factor 3 (ISGF3) complex [1]. IRF9 is best characterized as a transcription factor that mediates (as part of ISGF3) the type I interferon (IFN) response by regulating the downstream expression of interferon-stimulated genes (ISGs) [5, 6]. In the initial activation phase of innate antiviral immune response, activated TLR induces the production of early phase NF-κBdependent proinflammatory cytokines, the mitogen-activated protein kinases, and the IRF-dependent antiviral cytokines (i.e., type I IFNs) [reviewed in Ref.
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