Together with IFNAR2, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) . 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 . 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 . The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors . STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes . 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). .

P17181

Interferon alpha/beta receptor 1 (IFN-R-1) (IFN-alpha/beta receptor 1) (Cytokine receptor class-II member 1) (Cytokine receptor family 2 member 1) (CRF2-1) (Type I interferon receptor 1),IFNAR1 IFNAR,Interferon alpha/beta receptor 1, Cytokine receptor family 2 member 1, Cytokine receptor class-II member 1, CRF2-1, IFN-R-1, IFNAR1, IFNAR, IFN-alpha/beta receptor 1, Type I interferon receptor 1

Human

FC,ELISA

FC 1:50-1:200
ELISA 1:5000-1:20000

64kD

PerCP

Human

Monoclonal

SA365

IgG1, kappa

0.01M PBS, pH 7.4, 0.2% BSA, 0.05% Proclin 300.

0.5 mg/ml

Store at 4℃ for 12 months. Protect from light. Do not freeze.