Human Recombinant IFNAR2 protein, hFc Tag (V2LY-0526-LY5047)

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Basic Information

Expressed Host
HEK293 Cells
Protein Species
Human
Tag
hFc Tag
Protein Construction
This product is Human Recombinant IFNAR2 protein, hFc Tag consist of Amino Acid: 1-243 and predicts a molecular mass of 51.8 kDa.
Molecule Mass
51.8 kDa
Verified
HPLC
Sequence
Amino Acid: 1-243
Species
Human

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity
≥90% as determined by SDS-PAGE. ≥90% as determined by SEC-HPLC.
Endotoxin
Please contact us for more information.
Format
Lyophilized
Reconstitution
Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.
Buffer
Lyophilized from sterile Tris, NaCl, Glutathione, EDTA, DTT, PMSF, Glycerol
Preservative
None
Storage
Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
More Infomation

Target

Full Name
Interferon Alpha And Beta Receptor Subunit 2
Function
Associates with IFNAR1 to form the plasma membrane receptor in the type I interferon signaling pathway (PubMed:26424569, PubMed:28165510, PubMed:32972995).

Directly involved in signal transduction through its association with the TYR kinase JAK1 (PubMed:8181059, PubMed:7665574, PubMed:7759950).

Involved in interferon-mediated STAT1, STAT2 and STAT3 activation (PubMed:26424569, PubMed:32972995).

Isoform 3:
Potent inhibitor of type I IFN receptor activity.
Biological Process
Cell surface receptor signaling pathway Source: ProtInc
Cytokine-mediated signaling pathway Source: GO_Central
Defense response to virus Source: UniProtKB
Receptor signaling pathway via JAK-STAT Source: ProtInc
Response to interferon-alpha Source: UniProtKB
Response to interferon-beta Source: UniProtKB
Response to virus Source: ProtInc
Type I interferon signaling pathway Source: UniProtKB
Cellular Location
Isoform 1&2: Cell membrane
Isoform 3: Secreted
Involvement in disease
Immunodeficiency 45 (IMD45):
An autosomal recessive disorder characterized by increased susceptibility to viral infection due to impaired antiviral immunity, resulting in infection-associated encephalopathy. Affected individuals are at risk for developing fatal encephalitis after routine measles/mumps/rubella (MMR) vaccination.
Topology
Extracellular: 27-243
Helical: 244-264
Cytoplasmic: 265-515
PTM
Phosphorylated on tyrosine residues upon interferon binding. Phosphorylation at Tyr-337 or Tyr-512 are sufficient to mediate interferon dependent activation of STAT1, STAT2 and STAT3 leading to antiproliferative effects on many different cell types.
Glycosylated.

Duncan, C. J., Skouboe, M. K., Howarth, S., Hollensen, A. K., Chen, R., Børresen, M. L., ... & Mogensen, T. H. (2022). Life-threatening viral disease in a novel form of autosomal recessive IFNAR2 deficiency in the Arctic. Journal of Experimental Medicine, 219(6), e20212427.

Dieter, C., de Almeida Brondani, L., Lemos, N. E., Schaeffer, A. F., Zanotto, C., Ramos, D. T., ... & Crispim, D. (2022). Polymorphisms in ACE1, TMPRSS2, IFIH1, IFNAR2, and TYK2 genes are associated with worse clinical outcomes in COVID-19. Genes, 14(1), 29.

Fricke-Galindo, I., Martínez-Morales, A., Chávez-Galán, L., Ocaña-Guzmán, R., Buendía-Roldán, I., Pérez-Rubio, G., ... & Falfán-Valencia, R. (2022). IFNAR2 relevance in the clinical outcome of individuals with severe COVID-19. Frontiers in Immunology, 13, 949413.

Meyts, I. (2022). Null IFNAR1 and IFNAR2 alleles are surprisingly common in the Pacific and Arctic.

Zhang, L., Ma, J., Jin, X., Zhang, L., Zhang, M., Li, P. Z., ... & Zhang, L. (2022). Human IFNAR2 Mutant Generated by CRISPR/Cas9-Induced Exon Skipping Upregulates a Subset of Tonic-Like Interferon-Stimulated Genes Upon IFNβ Stimulation. Journal of Interferon & Cytokine Research, 42(11), 580-589.

Akter, S., Roy, A. S., Tonmoy, M. I. Q., & Islam, M. S. (2022). Deleterious single nucleotide polymorphisms (SNPs) of human IFNAR2 gene facilitate COVID-19 severity in patients: a comprehensive in silico approach. Journal of Biomolecular Structure and Dynamics, 40(21), 11173-11189.

Shemesh, M., Lochte, S., Piehler, J., & Schreiber, G. (2021). IFNAR1 and IFNAR2 play distinct roles in initiating type I interferon–induced JAK-STAT signaling and activating STATs. Science signaling, 14(710), eabe4627.

Smieszek, S. P., Polymeropoulos, V. M., Xiao, C., Polymeropoulos, C. M., & Polymeropoulos, M. H. (2021). Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susceptibility. Journal of Global Antimicrobial Resistance, 26, 239-240.

Passarelli, C., Civino, A., Rossi, M. N., Cifaldi, L., Lanari, V., Moneta, G. M., ... & Prencipe, G. (2020). IFNAR2 deficiency causing dysregulation of NK cell functions and presenting with hemophagocytic lymphohistiocytosis. Frontiers in Genetics, 11, 937.

Shepardson, K. M., Larson, K., Johns, L. L., Stanek, K., Cho, H., Wellham, J., ... & Rynda-Apple, A. (2018). IFNAR2 is required for anti-influenza immunity and alters susceptibility to post-influenza bacterial superinfections. Frontiers in immunology, 9, 2589.

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For research use only. Not intended for any clinical use.

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