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AB56070

Anti-IFNAR2 antibody

4

(1 Review)

|

(10 Publications)

Rabbit Polyclonal IFNAR2 antibody. Suitable for ELISA, WB, ICC/IF and reacts with Human samples. Cited in 10 publications. Immunogen corresponding to Synthetic Peptide within Human IFNAR2.

View Alternative Names

IFNABR, IFNARB, IFNAR2, Interferon alpha/beta receptor 2, IFN-R-2, IFN-alpha binding protein, IFN-alpha/beta receptor 2, Interferon alpha binding protein, Type I interferon receptor 2

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

ICC/IF, WB, ELISA

applications

Immunogen

Synthetic Peptide within Human IFNAR2. The exact immunogen used to generate this antibody is proprietary information.

P48551

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Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "ELISA" : {"fullname" : "ELISA", "shortname":"ELISA"}, "WB" : {"fullname" : "Western blot", "shortname":"WB"}, "ICCIF" : {"fullname" : "Immunocytochemistry/ Immunofluorescence", "shortname":"ICC/IF"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "ELISA-species-checked": "guaranteed", "ELISA-species-dilution-info": "", "ELISA-species-notes": "<p></p>", "WB-species-checked": "guaranteed", "WB-species-dilution-info": "", "WB-species-notes": "<p>Two hour incubation. This antibody has been tested in Western blot against the recombinant peptide used as an immunogen. We have no data on detection of endogenous protein.</p>", "ICCIF-species-checked": "guaranteed", "ICCIF-species-dilution-info": "", "ICCIF-species-notes": "<p></p>" } } }
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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Purification notes
Purified by antigen specific affinity chromatography.
Storage buffer
pH: 7.2 Preservative: 0.01% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine)
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
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Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

IFNAR2 also known as Interferon Alpha/Beta Receptor 2 is a critical part of the immune system. It pairs with IFNAR1 to form the receptor complex binding type I interferons such as IFN-alpha and IFN-beta. The IFNAR2 protein itself weighs roughly 60 kDa. You can find it expressed on the surface of almost all cell types making it a versatile participant in cellular immune responses. Cellular assays such as IFN-alpha ELISA often use IFNAR2 to quantify type I interferon activity and researchers frequently study it to understand its role in immune regulation.
Biological function summary

IFNAR2 plays a role in mediating the effects of type I interferons. It forms part of a receptor complex with IFNAR1 to initiate signal transduction upon binding to its ligands leading to activation of the JAK-STAT signaling pathway. This pathway then induces the expression of interferon-stimulated genes (ISGs) that promote antiviral defense cell growth control and modulation of the immune response. Without the function of IFNAR2 within this complex cells would be unable to respond appropriately to viral infections.

Pathways

IFNAR2 is widely recognized in its involvement with the JAK-STAT pathway. Through this pathway IFNAR2 interacts closely with various proteins like JAK1 and STAT1 propagating the signal that leads to the transcription of numerous ISGs. Another vital pathway involving IFNAR2 is the induction of cytokines which influences the adaptive immune response. Its position within these pathways illustrates its functional importance in antiviral defense and immune system regulation.

IFNAR2 has associations with multiple sclerosis and systemic lupus erythematosus. In multiple sclerosis type I interferon pathways mediated by IFNAR2 can modulate immune responses implicated in the progression of this neurodegenerative disorder. Increased IFNAR2 activity might exacerbate lupus characterized by improper immune system regulation. IFN-alpha a cytokine closely linked to IFNAR2 plays a pivotal role in these conditions highlighting its importance in disease development and potential therapeutic targeting.
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Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:
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Target data

Together with IFNAR1, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) (PubMed : 10049744, PubMed : 10556041, PubMed : 21854986, PubMed : 26424569, PubMed : 28165510, PubMed : 32972995, PubMed : 7665574, PubMed : 7759950, PubMed : 8181059, PubMed : 8798579, PubMed : 8969169). 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 (PubMed : 10049744, PubMed : 17517919, PubMed : 21854986, PubMed : 26424569, PubMed : 28165510, PubMed : 32972995, PubMed : 7665574, PubMed : 7759950, PubMed : 8181059, PubMed : 8798579, PubMed : 8969169). 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 (PubMed : 10556041, PubMed : 11682488, PubMed : 12105218, PubMed : 21854986, PubMed : 32972995). The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors (STAT1, STAT2 and STAT) (PubMed : 11682488, PubMed : 12105218, PubMed : 21854986, PubMed : 32972995). STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes (PubMed : 12105218, PubMed : 28165510, PubMed : 9121453).. Isoform 3. Potent inhibitor of type I IFN receptor activity.
See full target information IFNAR2
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Publications (10)

Recent publications for all applications. Explore the full list and refine your search

JCI insight 10: PubMed40892477

2025

Type I IFNs enhance human dorsal root ganglion nociceptor excitability and induce TRPV1 sensitization.

Applications

Unspecified application

Species

Unspecified reactive species

Úrzula Franco-Enzástiga,Keerthana Natarajan,Felipe Espinosa,Rafael Granja-Vazquez,Hemanth Mydugolam,Theodore J Price

EBioMedicine 70:103477 PubMed34284174

2021

Expression characteristics of interferon-stimulated genes and possible regulatory mechanisms in lupus patients using transcriptomics analyses.

Applications

Unspecified application

Species

Unspecified reactive species

Yiyao Deng,Ying Zheng,Delun Li,Quan Hong,Min Zhang,Qinggang Li,Bo Fu,Lingling Wu,Xu Wang,Wanjun Shen,Yingjie Zhang,Jiakai Chang,Kangkang Song,Xiaomin Liu,Shunlai Shang,Guangyan Cai,Xiangmei Chen

PLoS genetics 16:e1009199 PubMed33104735

2020

Function of multiple sclerosis-protective HLA class I alleles revealed by genome-wide protein-quantitative trait loci mapping of interferon signalling.

Applications

Unspecified application

Species

Unspecified reactive species

Christian Lundtoft,Pascal Pucholt,Juliana Imgenberg-Kreuz,Jonas Carlsson-Almlöf,Maija-Leena Eloranta,Ann-Christine Syvänen,Gunnel Nordmark,Johanna K Sandling,Ingrid Kockum,Tomas Olsson,Lars Rönnblom,Niklas Hagberg

Nature neuroscience 22:1046-1052 PubMed31182869

2019

Central nervous system regeneration is driven by microglia necroptosis and repopulation.

Applications

Unspecified application

Species

Unspecified reactive species

Amy F Lloyd,Claire L Davies,Rebecca K Holloway,Yasmine Labrak,Graeme Ireland,Dario Carradori,Alessandra Dillenburg,Eva Borger,Daniel Soong,Jill C Richardson,Tanja Kuhlmann,Anna Williams,Jeffrey W Pollard,Anne des Rieux,Josef Priller,Veronique E Miron

The Canadian journal of cardiology 35:875-883 PubMed31292086

2019

Role of the mTOR Signalling Pathway in Human Sepsis-Induced Myocardial Dysfunction.

Applications

Unspecified application

Species

Unspecified reactive species

Wei Cheng Mm,Yun Long,Hao Wang,Wen Han Mm,Jiahui Zhang,Na Cui

The Journal of biological chemistry 293:5975-5986 PubMed29496996

2018

Interferon down-regulation of miR-1225-3p as an antiviral mechanism through modulating Grb2-associated binding protein 3 expression.

Applications

Unspecified application

Species

Unspecified reactive species

Min Cheng,Yuqiang Niu,Jingjing Fan,Xiaojing Chi,Xiuying Liu,Wei Yang

Experimental and therapeutic medicine 14:5924-5930 PubMed29285141

2017

Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus.

Applications

Unspecified application

Species

Unspecified reactive species

Qian Yang,Xiao-Peng Li,Yuan-Bin Zhong,Tian-Xin Xiang,Lun-Li Zhang

Molecular cancer therapeutics 13:948-61 PubMed24526161

2014

Interferon-β induces loss of spherogenicity and overcomes therapy resistance of glioblastoma stem cells.

Applications

Unspecified application

Species

Unspecified reactive species

Caroline Happold,Patrick Roth,Manuela Silginer,Ana-Maria Florea,Katrin Lamszus,Karl Frei,Rene Deenen,Guido Reifenberger,Michael Weller

The Journal of biological chemistry 288:16196-205 PubMed23599426

2013

Innate immunity in pluripotent human cells: attenuated response to interferon-β.

Applications

Unspecified application

Species

Human

Xiao-Xiao Hong,Gordon G Carmichael

Proceedings of the National Academy of Sciences of the United States of America 105:11673-8 PubMed18687895

2008

A link between SIN1 (MAPKAP1) and poly(rC) binding protein 2 (PCBP2) in counteracting environmental stress.

Applications

IP

Species

Human

Debjani Ghosh,Gyan P Srivastava,Dong Xu,Laura C Schulz,R Michael Roberts
View all publications
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