Render Target: STATIC
Render Timestamp: 2024-12-12T11:04:15.581Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-11-05 22:31:10.271
Product last modified at: 2024-12-02T12:30:08.860Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

IFNAR2 (E7R3A) Rabbit mAb #80537

Filter:
  • WB

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa) 40-100
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:10 - 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    IFNAR2 (E7R3A) Rabbit mAb recognizes endogenous levels of total IFNAR2 protein. This clone recognizes isoforms 1, 2, and 3 of mouse IFNAR2 protein.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of mouse IFNAR2 protein.

    Background

    Interferon alpha/beta receptor 2 (IFNAR2) is one of the two protein subunits that comprise the type I interferon (IFN-I) surface receptor. IFNAR2 is a class II helical cytokine receptor with an ectodomain composed of two fibronectin type III-like subdomains, D1 and D2, and an unstructured intracellular domain (ICD) (1,2). IFNAR2 is expressed on most nucleated cells (3). IFN-Is bind the IFN receptor, leading to the dimerization of IFNAR2 and IFNAR1 subunits, and the activation of Janus family kinase (JAK) and signal transducer and activator of transcription (STAT) signaling pathways (4,5). JAK1 is associated with IFNAR2, and STAT1 and STAT2 are constitutively bound to the intracellular domain (ICD) of IFNAR2 (6,7). The formation of the transcription factor IFN-stimulated gene factor 3 (ISGF3), which is a complex made up of the pSTAT1-pSTAT2 heterodimer and interferon regulatory factor 9 (IRF-9), leads to the transcription of interferon-stimulated genes (ISGs) (8). IFN-I subtypes have differential binding affinity toward IFNAR2, contributing to differences in response potency (9). In contrast, IFN-αs all bind IFNAR1 with a low affinity and only IFN-β binds IFNAR1 with a relatively higher affinity (10). IFN-I signaling mediates various cellular responses, including antiviral responses, immunomodulatory responses, and antiproliferative effects (3). In the tumor microenvironment (TME), the presence of IFN-I signaling is associated with “hot” tumors in which key effector immune cells are present and is predictive of therapeutic response, whereas suppressed IFN-I signaling in the TME is associated with tumor progression and poorer outcomes (11,12). IFN-I signaling is being investigated as a therapeutic target for cancer, autoimmunity, sepsis, and viral infection (13,14).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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