IFN-alpha/beta R2 Protein, Mouse (Biotinylated, HEK293, His, Avi)

The IFN-alpha/beta R2 Protein, in conjunction with IFNAR1, constitutes the heterodimeric receptor for type I interferons, encompassing interferons alpha, beta, epsilon, omega, and kappa. Upon type I interferon binding, the receptor activation initiates the JAK-STAT signaling cascade, leading to the transcriptional activation or repression of interferon-regulated genes that mediate the interferon response. Mechanistically, the binding of type I interferon brings IFNAR1 and IFNAR2 into close proximity, facilitating cross-phosphorylation of their associated Janus kinases (JAKs), with TYK2 bound to IFNAR1 and JAK1 bound to IFNAR2. The activated JAKs then phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, creating docking sites for STAT transcription factors (STAT1, STAT2, and STAT). These phosphorylated STAT proteins translocate into the nucleus, regulating the expression of interferon-regulated genes. Additionally, IFN-alpha/beta R2 proteins may function as potent inhibitors of type I interferon receptor activity, showcasing their role in modulating the interferon signaling pathway.