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Validated All-in-One™ qPCR Primer for IFNAR1(NM_000629.2) Search again
Product ID:
HQP009458
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AVP, IFN-alpha-REC, IFNAR, IFNBR, IFRC, IMD106
Gene Description:
interferon alpha and beta receptor subunit 1
Target Gene Accession:
NM_000629.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- Only the tyrosine-phosphorylated form of interferon alpha receptor subunit 1 binds to Stat2.
- Data show that Tyk2 tyrosine kinase is essential for stable cell surface expression of IFNAR1.
- Measles virus suppresses interferon-alpha signaling pathway: association of viral accessory proteins, C and V, with interferon-alpha receptor complex
- An association has been demonstrated between two IFNAR1 polymorphisms and cerebral malaria.
- IFNAR1 interacts with the Homolog of Slimb (HOS) F-box protein in a phosphorylation-dependent manner, and that this interaction is promoted by interferon alpha
- IFNAR1 and IFNAR2 levels reveal that the KAS-6/1 cell line overexpresses IFNAR1 relative to other myeloma cell lines that are growth arrested by IFN-alpha.
- phosphorylation and ubiquitin acceptor sites are required for ubiquitination and degradation of IFNAR1
- A dynamic model for the IFN-alpha/receptor complex predicts that IFNAR1 and IFNAR2 are probably anchored in close proximity on the cell surface and that upon IFN binding, the complex assumes a closed form, resulting in activation of intracellular kinases
- The IFNAR1 subunit of the type I IFN receptor complex contains a functional nuclear localization sequence.
- analysis of the roles of the four Ig-like sub-domains (SDs) of the extracellular domain of ifnar1 (ifnar1-EC) for ligand recognition and receptor assembling
- The promoter GT repeat dinucleotide microsatellite polymorphism of the IFNAR1 gene may represent a risk factor for the development of depressive symptoms during IFN-alpha therapy for hepatitis C and other conditions.
- Data describe the mapping of the complete binding region of IFNAR1 on IFNalpha2 using a panel of 21 single alanine mutant proteins.
- Monocyte-derived dendritic cells can modulate their sensitivity to two IFN subtypes through a differential regulation of the IFNAR subunits.
- Human type I interferon receptor binding site on human interferon-alpha2 by cross saturation and an NMR-based model of the complex.
- Polymorphisms of IFNAR1 promoter may affect, at least in part, the outcomes of HBV infection.
- constructed a phage display library by randomizing three positions on IFNalpha2 previously shown to confer weak binding to IFNAR1
- Data describe the species specificity of IFN-alphas, the residues in murine IFN-alpha4 that preclude strong affinity interactions with human IFNAR1 and 2, and residues in human IFN-alpha8 that resemble a receptor interactive domain in murine IFN-alpha4.
- The intensity and distribution of IFNAR-1 may predict the response to therapy with IFN-alpha and IFN-beta in pancreatic cancer.
- This study suggests that when combination therapy with high dose IFN-alpha and ribavirin is administered, HCV genotypes and age rather than the IFNAR1 polymorphisms are the predictors of a sustained response.
- report that in response to type 1 interferon (IFNalpha), IFNalpha type 1 receptors recruit cytoplasmic CREB-binding protein (CBP).
- Ubiquitination of IFNAR1 promotes its interaction with the adaptin complex that is required for the robust internalization of IFNAR1, implicating cooperation between site-specific ubiquitination and the linear endocytic motif in regulating this process.
- We discuss the signaling events that might lead to ubiquitination and degradation of IFNAR1 via ligand-dependent and independent pathways and their potential physiologic significance.
- An IFNAR1/retinoic acid-inducible gene I (RIG-I)-dependent pathway mediates SOCS1 and SOCS3 up-regulation in influenza A virus-infected bronchial epithelial cells.
- place TRAF2 directly in the signaling pathway transduced through the IFNAR1 subunit of the IFN receptor
- Tyk2 contributes to both the regulation of total IFNAR1 levels as well as the regulation of the cell surface density of this receptor chain.
- a major bottleneck was observed during POLIOVIRUS transit to the brain in PVR mice, but was absent in PVR-IFNAR-/- mice, suggesting that the interferon response was a determinant of the peripheral site-to-brain bottleneck
- In conclusion, IFNAR1 19158C/G polymorphism is primarily associated with susceptibility to chronic HBV infection.
- the stability of the ternary interferon-receptor complex rather than the affinity to the individual subunits dictates differential biological activities
- Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 generates type I IFN competitive antagonists.
- CD11c-Cre+/- ifnar1(fl/fl) transgenic mice respond with vigorous IFN-alpha production to mouse hepatitis virus infection, suggesting that lack of IFNAR on plasmacytoid dendritic cells has no significant impact on the early type I IFN response.