anti-IFNAR2 (IFNAR2) 抗体产品概述

Pig (Porcine) Interferon alpha/beta Receptor 2 (IFNAR2) interaction partners

1. Here, the authors found that the interferon-alpha/beta receptor beta chain (IFNAR2) was down-regulated, while miR-30c was up-regulated during porcine respiratory and reproductive syndrome virus infection.

2. These results suggest that endometrial and conceptus IFNAR1 and IFNAR2 may mediate the action of type I IFNs during the implantation period for the establishment and maintenance of pregnancy in pigs.

3. The genomic structure of porcine IFNAR2 gene consists of nine exons and eight introns and mRNA expression was detected in all tissues examined

Mouse (Murine) Interferon alpha/beta Receptor 2 (IFNAR2) interaction partners

1. A role for IFNAR2 in induction of anti-IAV immune responses.

2. 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.

3. We found that STAT-1(-/-) MRL lpr m, but not IRF-9(-/-) or IFNAR-2(-/-) mice, developed interstitial nephritis characterized by infiltration with RORgammat-positive lymphocytes, macrophages, and eosinophils.

4. mTORC2 has a central role in IFNgamma signaling and type II IFN responses

5. In this study, we elucidate the in vivo importance of the soluble type I IFNAR, soluble (s)IFNAR2a

6. In this study we have characterized the Stat2-IFNaR2 interaction and examined its role in IFNalpha signaling

7. regions in promoter that confer basal and inducible expression

8. studies reveal that a single conserved IFNAR2 tyrosine, Y(510), plays a critical role in directing the IFN-I-dependent activation of STAT1 and STAT2, both in murine fibroblasts and macrophages

9. The local transgenic expression of GM-CSF in the stomach overrides any possible modulatory effects of IFNAR2 on experimental autoimmune gastritis development.

10. Data show that that DC, especially the CD8alpha(+) subset, from type I IFN receptor knock out (IFNAR KO) mice, display a reduced turnover rate when compared with DC from WT mice.

11. Our studies provide a critical link between the IFN-I pathway and the regulation of TLR-specific B-cell responses in a murine model of Systemic lupus erythematosus

12. ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3, but not NF-kappaB. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila

Human Interferon alpha/beta Receptor 2 (IFNAR2) interaction partners

1. 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.

2. 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.

3. Report lowered serum IFNAR2 levels in multiple sclerosis patients are elevated on treatment with interferon-beta.

4. 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.

5. 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

6. A very small percentage of the pancreatic tumors showed strong expression of the IFNAR-2c.

7. 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.

8. The expression of IFNAR1, IFNgammaR1 and ribovarin transporters were significantly impaired in chronic liver disease and cirrhotic livers.

9. 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.

10. Dimerization of IFNAR1 and IFNAR2 and the limiting role of IFNAR1 binding affinity in complex assembly is modulated by USP18.

11. 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.

12. 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.

13. 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.

14. IFNAR2 overexpression was observed in various histological types of lung cancer, and appears to be associated with lung cancers that behave aggressively.

15. 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.

16. 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

17. In this study we have characterized the Stat2-IFNaR2 interaction and examined its role in IFNalpha signaling

18. STAT3 activation by type I interferons is dependent on specific tyrosines located in the cytoplasmic domain of interferon receptor chain 2c

19. Expression and signaling activity of interferon alpha/beta receptors modulates dendritic cell (DC) responsiveness during terminal maturation and differentiation of monocyte-derived DCs.

20. Subunit 2 of the interferon alpha receptor (IFNaR2) is bound more avidly to Stat2 than is phosphorylated IFNaR1.