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we uncovered that IFNAR1 expression in stromal benign cells functions to protect against progression of leukemia.
Concurrent ablation of Ifnar1 led to a modest attenuation of the CK1alpha (zeige CSNK1A1 Proteine)-null phenotype indicating that, although other CK1alpha (zeige CSNK1A1 Proteine) targets are likely to be important, IFNAR1 downregulation can contribute to the maintenance of the HSCs function.
Central nervous system signaling through IFNAR1 is a factor that is critical to neural injury after stroke.
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 (zeige APP Proteine) 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 (zeige IFNA Proteine)/beta to produce alloantibodies to the human KEL glycoprotein in mice.
These data suggest that plasmacytoid dendritic cells producing IFN-alpha (zeige IFNA Proteine) and IL-33 (zeige IL33 Proteine) 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 (zeige CCL1 Proteine) expression including CCL2 (zeige CCL2 Proteine).
this study shows that the presence of IFN-alpha (zeige IFNA Proteine) at antigen sensitization activates an IDO1 (zeige IDO1 Proteine)/TGF-beta (zeige TGFB1 Proteine)-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 (zeige TYR Proteine)(240) and Tyr (zeige TYR Proteine)(274) interacting with IFN-beta (zeige IFNB1 Proteine) residues Phe(63), Leu(64), Glu (zeige GCG Proteine)(77), Thr (zeige TRH Proteine)(78), Val(81), and Arg(82) that underlie IFN-beta (zeige IFNB1 Proteine)-IFNAR1-mediated signaling and biological processes.
Relapsing-remitting multiple sclerosis patients manifested a statistically higher expression level of IFNAR1 than their normal counterparts.
cellular kinase, casein kinase 1alpha (CK1alpha (zeige CSNK1A1 Proteine)), is crucial for IAV HA-induced degradation of both IFNGR1 (zeige IFNGR1 Proteine) and IFNAR1.
The authors find that UCHL3 (zeige Uchl3 Proteine) regulates COPS5 (zeige COPS5 Proteine)-dependent deneddylation of Cullin1, which is an essential component of SCF (zeige KITLG Proteine)(beta-TrCP (zeige BTRC Proteine)) complex and associated with SCF (zeige KITLG Proteine)(beta-TrCP (zeige BTRC Proteine)) activities. The authors further demonstrate that UCHL3 (zeige Uchl3 Proteine) upregulates the levels of SCF (zeige KITLG Proteine)(beta-TrCP (zeige BTRC Proteine)) substrates including IFN-I receptor IFNAR1, which enhances IFN-I mediated signaling pathway and antiviral activity.
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 (zeige MMP9 Proteine) in infected patients and leukocytes. On the other hand, MMP-9 (zeige MMP9 Proteine) facilitates hepatitis B virus replication through repressing IFN/JAK (zeige JAK3 Proteine)/STAT (zeige STAT1 Proteine) signaling, IFNAR1 function, and IFN-alpha (zeige IFNA Proteine) action.
this study shows that single nucleotide polymorphism in IFNAR1 gene is associated with female vitiligo (zeige MITF Proteine) in Estonian patients
A small proportion of both pancreatic and periampullary tumors showed a strong expression of the IFNAR-1.
Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 (zeige IFNA2 Proteine) 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