Anti-Human IFNAR1 Recombinant Antibody (64G12) (HB823013)

Name: Anti-Human IFNAR1 Recombinant Antibody (64G12)
Brand: abinScience
SKU: HB823013
Price: 196 USD
Availability: InStock

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50ug
100ug
1mg

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Overview
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References
Datasheet
SDS

Overview

Catalog No.

HB823013

Species reactivity

Human

Applications

ELISA, SPR

Host species

Mouse

Isotype

IgG2a, kappa

Clone ID

64G12

Clonality

Monoclonal

Target

IFNAR1, Interferon alpha/beta receptor 1, IFN-alpha/beta receptor 1, Cytokine receptor class-II member 1, Cytokine receptor family 2 member 1, CRF2-1, Type I interferon receptor 1

Endotoxin level

Please contact with the lab for this information.

Purity

>95% as determined by SDS-PAGE.

Purification

Protein A/G purified from cell culture supernatant.

Accession

P17181

RRID

Anti-Human IFNAR1 Antibody (64G12) (abinScience Cat# HB823013, RRID:AB_3727131)

Form

Liquid

Storage buffer

0.01M PBS pH 7.4

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

Product Usage Information

Application	Dilution
ELISA	1:2000-1:20000

Stability and Storage

Use a manual defrost freezer and avoid repeated freeze-thaw cycles. Store at 4°C short term (1-2 weeks). Store at -20°C 12 months. Store at -80°C long term.

Background

Interferon alpha/beta receptor 1 (IFNAR1) is a ~63 kDa protein. Together with IFNAR2, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa). Type I interferon binding activates the JAK-STAT signaling cascade, resulting in transcriptional activation or repression of interferon-regulated genes that encode the effectors of the interferon response. Mechanistically, type I interferon-binding brings the IFNAR1 and IFNAR2 subunits into close proximity with one another, driving their associated Janus kinases (JAKs) (TYK2 bound to IFNAR1 and JAK1 bound to IFNAR2) to cross-phosphorylate one another. The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors. STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes.

1. Russell-Harde, D. et al. (1999) Biochemical and biophysical research communications 255, 539-44. PMID: 10049744

2. Kumar, KG. et al. (2003) The EMBO journal 22, 5480-90. PMID: 14532120

3. Kumar, KG. et al. (2004) The Journal of biological chemistry 279, 46614-20. PMID: 15337770

4. Uzé, G. et al. (1990) Cell 60, 225-34. PMID: 2153461

5. Thomas, C. et al. (2011) Cell 146, 621-32. PMID: 21854986

6. Zheng, H. et al. (2013) Cell reports 5, 180-93. PMID: 24075985

7. Hernandez, N. et al. (2019) The Journal of experimental medicine 216, 2057-2070. PMID: 31270247

8. Gothe, F. et al. (2022) Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 74, 136-139. PMID: 33252644

9. Bastard, P. et al. (2022) The Journal of experimental medicine 219. PMID: 35442418

10. Abramovich, C. et al. (1994) The EMBO journal 13, 5871-7. PMID: 7813427

Note

For research use only.

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