IFN-α is secreted by various cell types, stimulating macrophages and NK cells to trigger antiviral responses, and it also possesses antitumor activity. IFN-α acts as a pyrogen by altering the activity of thermosensitive neurons in the hypothalamus, leading to fever. Through a similar mechanism, IFN-α can be used to alleviate pain by interacting with μ-opioid receptors, acting as analgesics.All type I interferons (IFNs: IFN-α, IFN-β, IFN-ε, IFN-κ, and IFN-ω) bind to a common receptor on the surface of human cells, known as the type I IFN receptor. The type I IFN receptor consists of two subunits, IFNAR1 and IFNAR2, which associate with Janus-activated kinase (JAK) tyrosine kinase 2 (TYK2) and JAK1, respectively. Activation of JAK associated with the type I IFN receptor leads to the phosphorylation of STAT2 and STAT1, resulting in the formation of the STAT1-STAT2-IRF9 complex, known as ISGF3 (interferon-stimulated gene (ISG) factor 3) complex. These complexes translocate to the nucleus and bind to IFN-stimulated response elements in DNA to initiate gene transcription.IFNα Reporter MDCK Cell Line is a luciferase reporter cell line constructed based on the STAT signaling pathway. When interferon (recombinant canine α-interferon) binds to the canine type I IFN receptor (IFNAR1 and IFNAR2), it activates the signaling pathway, leading to the formation of the ISGF3 complex. The complex translocates to the nucleus and binds to the IFN-stimulated response elements in DNA, activating the expression of luciferase. The luciferase readout reflects the activation effect of the signaling pathway and can be used for in vitro evaluation of related drug effects.
