Anti-Interferon alpha/beta receptor 1 抗体

ターゲットの情報

Together with IFNAR2, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) (PubMed : 10049744, PubMed : 14532120, PubMed : 15337770, PubMed : 2153461, PubMed : 21854986, PubMed : 24075985, PubMed : 31270247, PubMed : 33252644, PubMed : 35442418, PubMed : 7813427). Type I interferon binding activates the JAK-STAT signaling cascade, resulting in transcriptional activation or repression of interferon-regulated genes that encode the effectors of the interferon response (PubMed : 10049744, PubMed : 21854986, PubMed : 7665574). Mechanistically, type I interferon-binding brings the IFNAR1 and IFNAR2 subunits into close proximity with one another, driving their associated Janus kinases (JAKs) (TYK2 bound to IFNAR1 and JAK1 bound to IFNAR2) to cross-phosphorylate one another (PubMed : 21854986, PubMed : 32972995, PubMed : 7665574, PubMed : 7813427). The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors (PubMed : 21854986, PubMed : 32972995, PubMed : 7526154, PubMed : 7665574, PubMed : 7813427). STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes (PubMed : 19561067, PubMed : 21854986, PubMed : 32972995, PubMed : 7665574, PubMed : 7813427, PubMed : 9121453). Can also act independently of IFNAR2 : form an active IFNB1 receptor by itself and activate a signaling cascade that does not involve activation of the JAK-STAT pathway (By similarity).