Anti-IFNAR1 Antibody (Rabbit Monoclonal antibody) General Information
Reacts with: Mouse
Recombinant Mouse IFNAR1 Protein (Catalog#50469-M08H)
This antibody was obtained from a rabbit immunized with purified, recombinant Mouse IFNAR1 (rM IFNAR1; Catalog#50469-M08H; NP_034638.2; Met1-Thr429).
Monoclonal Rabbit IgG Clone #110
0.2 μm filtered solution in PBS
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
Immunofluorescence staining of mouse IFNAR1 in mouse splenocytes. Cells were fixed with 4% PFA, blocked with 10% serum, and incubated with rabbit anti-mouse IFNAR1 monoclonal antibody (1:60) at 37℃ 1 hour. Then cells were stained with the Alexa Fluor® 594-conjugated Goat Anti-rabbit IgG secondary antibody (red) and counterstained with DAPI (blue).
Flow cytometric analysis of Mouse IFNAR1 expression on BABL/c splenocytes. Cells were stained with Mouse BD Fc Block™ purified anti-mouse CD16/CD32 mAb，then stained with purified anti-Mouse IFNAR1, then a FITC-conjugated second step antibody. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Interferon-alpha/beta receptor alpha chain (IFNAR1) is a type I membrane protein that forms one of the two chains of a receptor for interferons alpha and beta. Binding and activation of the receptor stimulates Janus protein kinases, which in turn phosphorylate several proteins, including STAT1 and STAT2. The encoded protein also functions as an antiviral factor. Tyk2 slows down IFNAR1 degradation and that this is due, at least in part, to inhibition of IFNAR1 endocytosis. Mutant versions of IFNAR1, in which Tyr466 is changed to phenylalanine, can act in a dominant negative manner to inhibit phosphorylation of STAT2. These observations are consistent with a model in which IFNAR1 mediates the interaction between JAK kinases and the STAT transcription factors.
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