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Gene Information

Gene symbol: IFNAR1

Gene name: interferon (alpha, beta and omega) receptor 1

HGNC ID: 5432

Synonyms: IFRC

Related Genes

# Gene Symbol Number of hits
1 CCR5 1 hits
2 CD4 1 hits
3 CD8A 1 hits
4 CLEC11A 1 hits
5 CREB3L4 1 hits
6 CTLA4 1 hits
7 CXCL10 1 hits
8 GZMB 1 hits
9 HIST1H3A 1 hits
10 HIST1H3H 1 hits
11 HLA-B 1 hits
12 HLA-DOB 1 hits
13 HLA-DRB1 1 hits
14 IFNA1 1 hits
15 IFNA14 1 hits
16 IFNA4 1 hits
17 IFNA5 1 hits
18 IFNA6 1 hits
19 IFNA8 1 hits
20 IFNB1 1 hits
21 IFNG 1 hits
22 IL1B 1 hits
23 IL6 1 hits
24 IL7R 1 hits
25 IRF9 1 hits
26 MAPK14 1 hits
27 MAPK4 1 hits
28 NET1 1 hits
29 PIK3C2A 1 hits
30 PRF1 1 hits
31 PTGS2 1 hits
32 TGFA 1 hits
33 TGFB1 1 hits
34 TNF 1 hits
35 TSPAN1 1 hits
36 ZNF395 1 hits

Related Sentences

# PMID Sentence
1 28604385 Importantly, IFN-γR-deficient BC-CML and AML were completely resistant to CD4- and CD8-mediated GVL, whereas IFN-γR/IFNAR1 double-deficient CP-CML was fully GVL sensitive.
2 27855206 However, whereas IFNAR KO mice showed infiltration by neutrophils and macrophages and higher expression of IL-1, IL-6 and Cox2, B6 WT mice show a cellular infiltration in the CNS composed predominantly of T cells, particularly CD8+ T cells, and increased mRNA expression levels of IFNg, GzmB and Prf1 at peak of disease.
3 25774455 Genes that were significantly regulated between VRs and VNRs were CREB3L4, HIST1H3A, HIST1H3H, IFNA1, IFNA4, IFNA5, IFNA6, IFNA8, IFNA14, IFNG, IFNAR1, IL6, IRF9, MAPK4, MAPK5, MAPK14, NET1, and PIK3C2A in the IFN array.
4 25774455 In the TLR array, only LBP and MAPK8 were found to be differentially regulated.
5 25774455 In the antigen processing array, HLA-A, HLA-C, HLA-DMA, HLA-DMB, HLA-F, PSMA5, PSMB8, and PSMB9 were differentially downregulated.
6 25445652 Interferon-γ (IFNG) microsatellite repeat and single nucleotide polymorphism haplotypes of IFN-α receptor (IFNAR1) associated with enhanced malaria susceptibility in Indian populations.
7 25445652 One SNP each from the IFNA8 and IFNA17 of IFNA gene cluster had a protective effect in the non-endemic region but not in the endemic region.
8 22295566 Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity.
9 22295566 Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity.
10 22295566 The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response.
11 22295566 The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response.
12 22295566 Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy.
13 22295566 Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy.
14 21628330 Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response.
15 21628330 The signaling adapters MyD88 and TRIF are engaged by TLRs and/or receptors of the IL-1 family and are considered important for innate immune responses that combat bacterial infections.
16 21628330 Here, the consequences of a combined MyD88 and TRIF deficiency for the innate immune response against severe septic peritonitis was examined.
17 21628330 We demonstrate that Myd88(-/-);Trif(Lps2/Lps2) mice had markedly reduced bacterial numbers in the peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is improved in the absence of MyD88/TRIF signals.
18 21628330 The lack of MyD88/TRIF signaling prevented the excessive production of inflammatory cytokines and of IL-10.
19 21628330 In contrast, Ifng mRNA was expressed at WT levels, and induction of Ifnb mRNA was reduced only by one-half.
20 21628330 Consistent with these findings, numerous IFN-regulated genes, including p47 and p65 GTPases, as well as CXCL10, were expressed in a MyD88/TRIF-independent manner.
21 21628330 The production of p47 GTPases and CXCL10 in septic peritonitis was found to be dependent on the presence of IFNAR1, but not IFN-γ, indicating a normal induction of the type I IFN response in Myd88(-/-);Trif(Lps2/Lps2) mice, despite attenuated IFN-β production.
22 21628330 Together, these results provide evidence that in severe septic peritonitis, the absence of MyD88 and TRIF balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN responses.