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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 (show APP Proteins) 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 (show IFNA Proteins)/beta to produce alloantibodies to the human KEL glycoprotein in mice.
These data suggest that plasmacytoid dendritic cells producing IFN-alpha (show IFNA Proteins) and IL-33 (show IL33 Proteins) 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 (show CCL1 Proteins) expression including CCL2 (show CCL2 Proteins).
this study shows that the presence of IFN-alpha (show IFNA Proteins) at antigen sensitization activates an IDO1 (show IDO1 Proteins)/TGF-beta (show TGFB1 Proteins)-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
These results identify a key interface created by IFNAR1 residues Tyr (show TYR Proteins)(240) and Tyr (show TYR Proteins)(274) interacting with IFN-beta (show IFNB1 Proteins) residues Phe(63), Leu(64), Glu (show GCG Proteins)(77), Thr (show TRH Proteins)(78), Val(81), and Arg(82) that underlie IFN-beta (show IFNB1 Proteins)-IFNAR1-mediated signaling and biological processes.
IFNAR1-deficiency accelerated humoral immune responses and parasite control by boosting ICOS (show ICOS Proteins)-signalling in two non-lethal murine models of malaria
reduced type I interferon (show IFNA Proteins) production in obesity is caused by SOCS3 (show SOCS3 Proteins) overexpression as well as tolerance induced by leptin (show LEP Proteins)
Downregulation of IFNAR1 promotes melanoma development and progression. IFNAR1 mutation, which is partially resistant to downregulation, delays melanoma development.
Low IFNAR1 expression is associated with peritoneal metastasis in gastric cancer.
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 (show MMP9 Proteins) in infected patients and leukocytes. On the other hand, MMP-9 (show MMP9 Proteins) facilitates hepatitis B virus replication through repressing IFN/JAK (show JAK3 Proteins)/STAT (show STAT1 Proteins) signaling, IFNAR1 function, and IFN-alpha (show IFNA Proteins) action.
this study shows that single nucleotide polymorphism in IFNAR1 gene is associated with female vitiligo (show MITF Proteins) in Estonian patients
A small proportion of both pancreatic and periampullary tumors showed a strong expression of the IFNAR-1.
rs2843710 of IFNAR1 was associated with the susceptibility and severity of EV71 HFMD in Chinese Han populations.
Genetic polymorphisms of the promoter of INFAR gene represent important factors associated with the clinical phase of HBeAg-negative chronic HBV infection.
data illustrate a lipid G-protein coupled receptor (GPCR (show TAS1R3 Proteins))-IFNAR1 regulatory loop that balances effective and detrimental immune responses and elevated endogenous S1PR1 (show S1PR1 Proteins) signaling
Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 (show IFNA2 Proteins) 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