Anti-IFN-alpha/beta R1 Polyclonal Antibody (HB823014)

Name: Anti-IFN-alpha/beta R1 Polyclonal Antibody
Brand: abinScience
SKU: HB823014
Price: 168 USD
Availability: InStock

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概要
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概要

カタログ番号

HB823014

説明

Anti-IFNAR1 Polyclonal Antibody (HB823014) is a rabbit polyclonal antibody detecting IFNAR1 in ELISA, IHC, WB. Suitable for Human.

Highlights

●Affinity Purified — Minimal background and high purity for reliable results.
●Multi-Application — Validated across multiple applications.

種反応性

Human

アプリケーション

ELISA, IHC, WB

宿主種

Rabbit

クローン性

Polyclonal

アイソタイプ

IgG

免疫原

E. coli - derived recombinant Human IFNAR1 (Lys28-Asn227).

ターゲット

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

精製

Purified by antigen affinity column.

アクセッション番号

P17181

形態

Liquid

保存バッファー

0.01M PBS, pH 7.4, 50% Glycerol, 0.05% Proclin 300.

データシートのハードコピーまたはロット固有のCOAに記載された具体的なバッファー情報を参照してください。

製品使用情報

アプリケーション	希釈
ELISA	1:5000-1:20000
IHC	1:50-1:500
WB	1:500-1:2000

安定性と保存

Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at -20 to -80°C for twelve months from the date of receipt.

背景

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

注意事項

For research use only.

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参考文献

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