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Recombinant Human IFNAR1/IFNAR Protein (Fc Tag)– MSE Supplies LLC

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Recombinant Human IFNAR1/IFNAR Protein (Fc Tag)

SKU: PKSH030696-100

  • £62400
  • Save £7000



Recombinant Human IFNAR1/IFNAR Protein (Fc Tag)

 

SKU # PKSH030696
Expression Host HEK293 Cells

 

Description

Synonyms AVP, CRF2-1, Cytokine Receptor Class-II Member 1, Cytokine Receptor Family 2 Member 1, IFN-Alpha/Beta Receptor 1, IFN-R-1, IFN-alpha-REC, IFNAR, IFNAR1, Interferon Alpha/Beta Receptor 1, Type I Interferon Receptor 1
Species Human
Expression Host HEK293 Cells
Sequence Met 1-Lys 436
Accession P17181-1
Calculated Molecular Weight 74.0 kDa
Observed Molecular Weight 100-120 kDa
Tag C-hFc
Bio-activity Not validated for activity
  

 

Properties

Purity > 88 % as determined by reducing SDS-PAGE.
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from sterile PBS, pH 7.4
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.


Background

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.