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anti-Mouse (Murine) IFNAR1 Antibodies:
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Human Polyclonal IFNAR1 Primary Antibody for CyTOF, FACS - ABIN4900075
Lin, Liao, Lin, Lin: Blocking of the alpha interferon-induced Jak-Stat signaling pathway by Japanese encephalitis virus infection. in Journal of virology 2004
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Cow (Bovine) Polyclonal IFNAR1 Primary Antibody for IHC (fro), IP - ABIN550131
Biron: Interferons alpha and beta as immune regulators--a new look. in Immunity 2001
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Human Monoclonal IFNAR1 Primary Antibody for FACS - ABIN4897143
Fuchs, Kaiser-Labusch, Bank, Ammann, Kolb-Kokocinski, Edelbusch, Omran, Ehl: Tyrosine kinase 2 is not limiting human antiviral type III interferon responses. in European journal of immunology 2016
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Human Monoclonal IFNAR1 Primary Antibody for FACS - ABIN4897145
Stone, Giugliano, Schnell, Cheng, Leahy, Golden-Mason, Gale, Rosen: Hepatitis C virus pathogen associated molecular pattern (PAMP) triggers production of lambda-interferons by human plasmacytoid dendritic cells. in PLoS pathogens 2013
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Human Monoclonal IFNAR1 Primary Antibody for FACS - ABIN4897147
Ramachandran, Yu, Dyczynski, Baskaran, Zhang, Lulla, Lulla, Saul, Nelander, Dimberg, Merits, Leja-Jarblad, Essand: Safe and Effective Treatment of Experimental Neuroblastoma and Glioblastoma Using Systemically Delivered Triple MicroRNA-Detargeted Oncolytic Semliki Forest Virus. in Clinical cancer research : an official journal of the American Association for Cancer Research 2016
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Human Monoclonal IFNAR1 Primary Antibody for CyTOF, FACS - ABIN4900073
Zhou, Huang, Poon, Chen, Chan, Ng, Guan, Watt, Lu, Yuen, Zheng: Functional dissection of an IFN-alpha/beta receptor 1 promoter variant that confers higher risk to chronic hepatitis B virus infection. in Journal of hepatology 2009
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Human Polyclonal IFNAR1 Primary Antibody for IHC, WB - ABIN361505
Kumar, Krolewski, Fuchs: Phosphorylation and specific ubiquitin acceptor sites are required for ubiquitination and degradation of the IFNAR1 subunit of type I interferon receptor. in The Journal of biological chemistry 2004
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Human Polyclonal IFNAR1 Primary Antibody for IF, IHC - ABIN6712242
Li, Xu, Ma, Sun, Fu, Hou: 17beta-estradiol enhances the response of plasmacytoid dendritic cell to CpG. in PLoS ONE 2010
myelinating dorsal root ganglia (DRG) explants obtained from interferon-alpha/beta receptor knock-out mice are productively infected by Zika virus.
Blocking IFNAR1 inhibits multiple myeloma-driven Treg expansion and immunosuppression.
data indicate that the cytotoxic effect of IFN-beta activation in CMEI contribute to the impairment of definitive erythropoiesis associated with Klf1 deprivation
IFNAR and RAG2 transgenic mice models show that enhanced reovirus virulence is related to maturation of the type-I interferon response and age-related mortality following reovirus infection
Male mice with Ifnar(-/-) may better recapitulate Zika virus in humans and provide insight into the mechanism of sexual transmission.
Only type-I interferon restricts viral replication of attenuated Measles virus (MV) Schwarz strain in mice, independently of the presence of hCD46 receptor.
A key role of the IL7 and Interferon type I receptor axis in the regulation of intratumoral t-cell functions and in the development of primary breast tumor growth and metastasis.
Data, including data from studies in knockout and double-knockout mice, suggest complex and sex-specific roles of Ifnar1 and Ifnar2 in type 1 diabetes (T1D); female NOD mice develop T1D in absence of both Ifnar1 and Ifnar2, whereas male mice do not.
we uncovered that IFNAR1 expression in stromal benign cells functions to protect against progression of leukemia.
Concurrent ablation of Ifnar1 led to a modest attenuation of the CK1alpha-null phenotype indicating that, although other CK1alpha targets are likely to be important, IFNAR1 downregulation can contribute to the maintenance of the HSCs function.
Central nervous system signaling through IFNAR1 is a factor that is critical to neural injury after stroke.
a deleterious role for the type-1 IFNs as key modulators of the early neuroinflammatory response and therefore the neuronal cell death in Parkinson's disease
results clearly demonstrate that: (i) MHV-68, MHV-72 and MHV-4556 differentially interact with intracellular signaling and dysregulate IFN signal transduction; (ii) MHV-68, MHV-72 and MHV-4556 degrade type I IFN receptor in very early stages of infection (2-4hpi), but not type III IFN receptor
Results show that removal of type-1 IFN signalling in the APPSWE/PS1DeltaE9 mouse model of AD confers a predominantly anti-inflammatory glial response and protects from cognitive decline. However this phenotype does not correlate with alterations in amyloid deposition and only a modest reduction in Abeta monomer levels.
transfusion-induced differentiation of IFNAR1(-/-) B cells into germinal center B cells and plasma cells was significantly reduced, compared to WT B cells. This study demonstrates that B cells require signaling from IFN-alpha/beta to produce alloantibodies to the human KEL glycoprotein in mice.
study provides evidence of STING activation in T cells, in which STING agonists not only provoke type I IFN production and IFN-stimulated gene expression, mirroring the response of innate cells, but are also capable of activating cell stress and death pathways.
These data suggest that plasmacytoid dendritic cells producing IFN-alpha and IL-33 play a pivotal role in the chronic fibro-inflammatory responses underlying murine autoimmune pancreatitis and human IgG4-related autoimmune pancreatitis.
type I interferons, besides their known antiviral properties, can initiate the recruitment and activation of leukocytes via induction of chemokine expression including CCL2.
this study shows that the presence of IFN-alpha at antigen sensitization activates an IDO1/TGF-beta-dependent anti-inflammatory program that upon antigenic rechallenge prevents inflammation via plasmacytoid dendritic cells
these studies demonstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 inhibition in scleroderma
Overexpression of IFNAR1, MX1 and signal transducer and activator of transcription 1 (Stat1) indicated the endogenous IFNa activation in tumour microenvironment, which correlated with immunosuppression status in head and neck squamous cell carcinomas (HNSCC) patients
results indicated that the IFNAR promoter methylation might have a potential relationship with the status of oxidative stress
Data suggest that IFNAR1-mediated expression of CH25H in healthy tissues limits the extent of education of these tissues by tumor-derived extracellular vesicles (TEV) and restricts the formation of the pre-metastatic niche in the lungs. Accordingly, these results suggest a defensive role of the IFNAR1-CH25H pathway against the development of distant lung metastases.
Our results show that levels of IFNAR-1 mRNA expression may be a good predictor for IFN-related anti-viral activity in both HCV mono infected and HCV/HBV co-infected patients.
A IFNAR1 protective variant, rs914142, is associated with lower expression of IFNAR1, whereas the Cerebral malaria (CM)-associated variant rs12626750 was associated with increased IFNAR1 expression, suggesting that activation of the type I IFN pathway may contribute to pathogenesis of CM.
The IFNAR-1 promoter polymorphisms are not involved in the expression levels of the main IFNAR-1 transcript. The -77VNTR has a regulatory role on the expression of a secondary, truncated, HCC-specific transcript, which in turn coincides with disruptions in cancer-associated pathways and in FN-1 expression modifications.
A digenic human immunodeficiency characterized by IFNAR1 and IFNGR2 mutations.
IFNAR1 signaling underlies an increased risk of tuberculosis in humans and reveals a function for the IFNAR1 inter-domain region in cytokine-cytokine receptor interaction and signal transduction.
HCV-1b core protein-induced miR-93-5p up-regulation inhibits the IFN signaling pathway by directly targeting IFNAR1, and the miR-93-5p-IFNAR1 axis regulates STAT1 phosphorylation.
Relapsing-remitting multiple sclerosis patients manifested a statistically higher expression level of IFNAR1 than their normal counterparts.
cellular kinase, casein kinase 1alpha (CK1alpha), is crucial for IAV HA-induced degradation of both IFNGR1 and IFNAR1.
The authors find that UCHL3 regulates COPS5-dependent deneddylation of Cullin1, which is an essential component of SCF(beta-TrCP) complex and associated with SCF(beta-TrCP) activities. The authors further demonstrate that UCHL3 upregulates the levels of SCF(beta-TrCP) substrates including IFN-I receptor IFNAR1, which enhances IFN-I mediated signaling pathway and antiviral activity.
Low IFNAR1 expression is associated with peritoneal metastasis in gastric cancer.
Here, we review the current knowledge on the main strategies that human pathogenic flaviviruses utilize to escape both type I IFN induction and effector pathways. [review]
the level of IFNAR1, IFNAR2, and CCR5 mRNA expression was found to be significantly lower in the responders than nonresponders.Our results highlighted the significance of IFNAR and CCR5 genes in multiple sclerosis risk and the response to IFN-b therapy.
Downregulation of IFNAR1 in tumor stroma stimulated colorectal cancer development and growth, played a key role in formation of the immune-privileged niche.
These results suggest that miR-29a, upregulated during RSV infection, is a negative regulator of IFNAR1 and is critical for respiratory syncytial virus NS1-induced virus replication.
On one hand, hepatitis B virus activates MMP-9 in infected patients and leukocytes. On the other hand, MMP-9 facilitates hepatitis B virus replication through repressing IFN/JAK/STAT signaling, IFNAR1 function, and IFN-alpha action.
this study shows that single nucleotide polymorphism in IFNAR1 gene is associated with female vitiligo in Estonian patients
A small proportion of both pancreatic and periampullary tumors showed a strong expression of the IFNAR-1.
Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 generates type I IFN competitive antagonists.
The complete 168,835 bp insert sequence of a porcine BAC clone harboring the IFNAR1 gene was determined.
The protein encoded by this gene 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.
interferon alpha/beta receptor 1
, interferon receptor
, soluble receptor
, interferon-alpha receptor 1
, putative interferon-alpha/beta receptor alpha chain
, interferon receptor 1
, interferon (alpha, beta and omega) receptor 1
, interferon alpha/beta receptor 1-like
, IFN-alpha/beta receptor 1
, INF-a receptor
, interferon-alpha/beta receptor 1
, type I interferon receptor 1
, alpha-type antiviral protein
, beta-type antiviral protein
, cytokine receptor class-II member 1
, cytokine receptor family 2 member 1
, interferon-alpha/beta receptor alpha chain
, interferon-beta receptor 1
, interferon (alpha and beta) receptor 1
, interferon, alpha; receptor
, Interferon-alpha/beta receptor alpha chain