Anti-Interferon alpha/beta receptor 1 antibody - BSA and Azide free,Abcam,AB10739
Endotoxin level is < 10 ng/mg antibody as determined by the LAL (Limulus amebocyte lysate) method. This antibody was used as a detection antibody in sELISA and was paired with ab91466 as capture antibody. Abreview 24657. IFNAR1 is a member of the cytokine receptor superfamily which also includes receptors for interleukins, IFN gamma, ciliary neurotrophic factor, somatotrophin, erythropoietin, nerve growth factor, tumor necrosis factor, leukemia inhibitory factor, and oncostatin M. Some members of the family have an alpha chain with either low or high ligand binding affinity and at least one beta chain involved in signal transduction with either relatively low or no ligand binding affinity. Type I interferons, alpha and beta, induce a variety of effects on target cells including antiviral, antiproliferative, and immunomodulatory activities. The alpha and beta interferons compete to bind to a common cell surface receptor, while IFN gamma binds to a distinct receptor. IFNAR1 is very responsive to type I interferons and bind to IFN beta and IFN alpha subtypes. It is also functionally involved in signal transduction because of its association with the cytoplasmic tyrosine kinase JAK1. The type I interferons, alpha and beta, are produced by leukocytes (alpha subunits), fibroblasts (beta subtypes), lymphocytes (omega subtypes), and ruminant embryos (tau subtypes). Interferon receptors are generally found on most human cell types whatever their origin, even on cells poorly responsive to interferon. IFNAR1 is expressed on the cell surface in a variety of human cell lines.
Host
Goat
Reactivity
Human
Application
ELISA, Flow Cyt, WB
Platform ID
BAB795441207
Abcam
Contact
Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215
Email:
Specifications
Scientific Background
Target data 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). See full target information IFNAR1
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