Mouse Monoclonal IFNAR2 antibody. Suitable for ELISA, WB and reacts with Human samples. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human IFNAR2.
Preservative: 0.1% Sodium azide
Constituents: PBS
| ELISA | WB | |
|---|---|---|
| Human | Expected | Expected |
| Species | Dilution info | Notes |
|---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
| Species | Dilution info | Notes |
|---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
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Together with IFNAR1, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) (PubMed:10049744, PubMed:10556041, PubMed:21854986, PubMed:26424569, PubMed:28165510, PubMed:32972995, PubMed:7665574, PubMed:7759950, PubMed:8181059, PubMed:8798579, PubMed:8969169). 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:17517919, PubMed:21854986, PubMed:26424569, PubMed:28165510, PubMed:32972995, PubMed:7665574, PubMed:7759950, PubMed:8181059, PubMed:8798579, PubMed:8969169). 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:10556041, PubMed:11682488, PubMed:12105218, PubMed:21854986, PubMed:32972995). The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors (STAT1, STAT2 and STAT) (PubMed:11682488, PubMed:12105218, PubMed:21854986, PubMed:32972995). STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes (PubMed:12105218, PubMed:28165510, PubMed:9121453). Isoform 3. Potent inhibitor of type I IFN receptor activity.
IFNABR, IFNARB, IFNAR2, Interferon alpha/beta receptor 2, IFN-R-2, IFN-alpha binding protein, IFN-alpha/beta receptor 2, Interferon alpha binding protein, Type I interferon receptor 2
Mouse Monoclonal IFNAR2 antibody. Suitable for ELISA, WB and reacts with Human samples. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human IFNAR2.
Preservative: 0.1% Sodium azide
Constituents: PBS
Reacts with both IFN-alpha2a and IFN-alpha2b
IFNAR2 also known as Interferon Alpha/Beta Receptor 2 is a critical part of the immune system. It pairs with IFNAR1 to form the receptor complex binding type I interferons such as IFN-alpha and IFN-beta. The IFNAR2 protein itself weighs roughly 60 kDa. You can find it expressed on the surface of almost all cell types making it a versatile participant in cellular immune responses. Cellular assays such as IFN-alpha ELISA often use IFNAR2 to quantify type I interferon activity and researchers frequently study it to understand its role in immune regulation.
IFNAR2 plays a role in mediating the effects of type I interferons. It forms part of a receptor complex with IFNAR1 to initiate signal transduction upon binding to its ligands leading to activation of the JAK-STAT signaling pathway. This pathway then induces the expression of interferon-stimulated genes (ISGs) that promote antiviral defense cell growth control and modulation of the immune response. Without the function of IFNAR2 within this complex cells would be unable to respond appropriately to viral infections.
IFNAR2 is widely recognized in its involvement with the JAK-STAT pathway. Through this pathway IFNAR2 interacts closely with various proteins like JAK1 and STAT1 propagating the signal that leads to the transcription of numerous ISGs. Another vital pathway involving IFNAR2 is the induction of cytokines which influences the adaptive immune response. Its position within these pathways illustrates its functional importance in antiviral defense and immune system regulation.
IFNAR2 has associations with multiple sclerosis and systemic lupus erythematosus. In multiple sclerosis type I interferon pathways mediated by IFNAR2 can modulate immune responses implicated in the progression of this neurodegenerative disorder. Increased IFNAR2 activity might exacerbate lupus characterized by improper immune system regulation. IFN-alpha a cytokine closely linked to IFNAR2 plays a pivotal role in these conditions highlighting its importance in disease development and potential therapeutic targeting.
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