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Significant associations were observed for 4 variants in IFNAR2, IFNLR1 with hepatitis B virus infection, and IFNLR1-rs4649203 was associated with hepatitis B recovery. Moreover, the authors demonstrated the clear relevance of 5 polymorphisms in IFNA1, IFNA2, IFNL4 with hepatocellular carcinoma.
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The findings underline the roles of UL36USP-IFNAR2 interaction in counteracting the type I IFN-mediated signaling pathway and reveal a novel evasion mechanism of antiviral innate immunity by HSV-1.
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Report lowered serum IFNAR2 levels in multiple sclerosis patients are elevated on treatment with interferon-beta.
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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.
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this study shows that the surface expression levels of the common IFN-alpha/beta receptor subunit 2 are significantly higher on plasmacytoid dendritic cells from females in comparison to males
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A very small percentage of the pancreatic tumors showed strong expression of the IFNAR-2c.
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Data suggest IFNA2 (interferon, alpha 2) binding to extracellular domain of IFNAR1 or IFNAR2 promotes proximity between intracellular domains; signaling depends on duration of activation/affinity of binding rather than specific conformational changes.
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The expression of IFNAR1, IFNgammaR1 and ribovarin transporters were significantly impaired in chronic liver disease and cirrhotic livers.
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Lack of expression of functional IFNAR2 does not seem to be the major cause of interferon resistance in hepatitis C virus patients receiving standard interferon therapy.
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Dimerization of IFNAR1 and IFNAR2 and the limiting role of IFNAR1 binding affinity in complex assembly is modulated by USP18.
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Therefore, this study associated, for the first time, in a large panel of pancreatic cancer cell lines the effects of IFN-alpha/-beta with the expression of type-I IFN receptors.
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Results suggest that oxidative stress play an important role in the regulation of type I interferon receptors IFNAR1 and IFNAR2 in chronic hepatitis B virus (HBV) infection.
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The effects of two functional polymorphisms, type I interferon receptor 2 gene (IFNAR2)-F8S and interleukin-10 receptor subunit beta gene (IL10RB)-K47E, on chronic hepatitis B virus (HBV) infection, were investigated.
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IFNAR2 overexpression was observed in various histological types of lung cancer, and appears to be associated with lung cancers that behave aggressively.
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A low number of receptors suffices for antiviral response and is thus a robust feature common to all cells. Conversely, a high number of receptors is required for antiproliferative activity, which allows for fine-tuning on a single-cell level.
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IFNAR1 (interferon-alpha receptor 1) (G/C in SNP18417) and IFNAR1 (interferon-alpha receptor 2) (G/T in SNP 11876) polymorphisms jointly, but not individually, may confer susceptibility to Behcets disease in a Turkish population
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In this study we have characterized the Stat2-IFNaR2 interaction and examined its role in IFNalpha signaling
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STAT3 activation by type I interferons is dependent on specific tyrosines located in the cytoplasmic domain of interferon receptor chain 2c
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Expression and signaling activity of interferon alpha/beta receptors modulates dendritic cell (DC) responsiveness during terminal maturation and differentiation of monocyte-derived DCs.
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Subunit 2 of the interferon alpha receptor (IFNaR2) is bound more avidly to Stat2 than is phosphorylated IFNaR1.