Aperçu des produits pour IFNAR1 Protéines (IFNAR1)

Mouse (Murine) Interferon (Alpha, beta and Omega) Receptor 1 (IFNAR1) interaction partners

1. myelinating dorsal root ganglia (DRG) explants obtained from interferon-alpha/beta receptor knock-out mice are productively infected by Zika virus.

2. Blocking IFNAR1 inhibits multiple myeloma-driven Treg expansion and immunosuppression.

3. data indicate that the cytotoxic effect of IFN-beta activation in CMEI contribute to the impairment of definitive erythropoiesis associated with Klf1 deprivation

4. 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

5. Male mice with Ifnar(-/-) may better recapitulate Zika virus in humans and provide insight into the mechanism of sexual transmission.

6. Only type-I interferon restricts viral replication of attenuated Measles virus (MV) Schwarz strain in mice, independently of the presence of hCD46 receptor.

7. 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.

8. 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.

9. we uncovered that IFNAR1 expression in stromal benign cells functions to protect against progression of leukemia.

10. 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.

11. Central nervous system signaling through IFNAR1 is a factor that is critical to neural injury after stroke.

12. 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

13. 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

14. 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.

15. 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.

16. 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.

17. 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.

18. type I interferons, besides their known antiviral properties, can initiate the recruitment and activation of leukocytes via induction of chemokine expression including CCL2.

19. 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

20. these studies demonstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 inhibition in scleroderma

Human Interferon (Alpha, beta and Omega) Receptor 1 (IFNAR1) interaction partners

1. results indicated that the IFNAR promoter methylation might have a potential relationship with the status of oxidative stress

2. 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.

3. 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.

4. 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.

5. 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.

6. A digenic human immunodeficiency characterized by IFNAR1 and IFNGR2 mutations.

7. 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.

8. 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.

9. Relapsing-remitting multiple sclerosis patients manifested a statistically higher expression level of IFNAR1 than their normal counterparts.

10. cellular kinase, casein kinase 1alpha (CK1alpha), is crucial for IAV HA-induced degradation of both IFNGR1 and IFNAR1.

11. 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.

12. Low IFNAR1 expression is associated with peritoneal metastasis in gastric cancer.

13. 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]

14. 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.

15. Downregulation of IFNAR1 in tumor stroma stimulated colorectal cancer development and growth, played a key role in formation of the immune-privileged niche.

16. 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.

17. 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.

18. this study shows that single nucleotide polymorphism in IFNAR1 gene is associated with female vitiligo in Estonian patients

19. A small proportion of both pancreatic and periampullary tumors showed a strong expression of the IFNAR-1.

20. rs2843710 of IFNAR1 was associated with the susceptibility and severity of EV71 HFMD in Chinese Han populations.

Cow (Bovine) Interferon (Alpha, beta and Omega) Receptor 1 (IFNAR1) interaction partners

1. Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 generates type I IFN competitive antagonists.

Pig (Porcine) Interferon (Alpha, beta and Omega) Receptor 1 (IFNAR1) interaction partners

1. The complete 168,835 bp insert sequence of a porcine BAC clone harboring the IFNAR1 gene was determined.