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Recombinant Human IFNAR1/IFNAR Protein (His Tag)
SKU: PKSH030695-100
Recombinant Human IFNAR1/IFNAR Protein (His Tag)
| SKU # | PKSH030695 |
| 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 | 48.6 kDa |
| Tag | C-His |
| Bio-activity | Not validated for activity |
Properties
| Purity | > 97 % 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.