Cat. # | Size | Qty. | Price |
---|---|---|---|
80537S | 100 µl |
|
REACTIVITY | M |
SENSITIVITY | Endogenous |
MW (kDa) | 40-100 |
Source/Isotype | Rabbit IgG |
Product Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Loading of prestained molecular weight markers (#59329, 10 µl/lane) to verify electrotransfer and biotinylated protein ladder (#7727, 10 µl/lane) to determine molecular weights are recommended.
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Mouse
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of mouse IFNAR2 protein.
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 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, IFNαs all bind IFNAR1 with a low affinity and only IFNβ binds IFNAR1 with a relatively higher affinity (10). IFN-I signaling mediates various cellular responses, including antiviral responses, immunomodulatory responses, and antiproliferative effects (11). 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 (12,13). IFN-I signaling is being investigated as a therapeutic target for cancer, autoimmunity, sepsis, and viral infection (14,15).
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