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Validated All-in-One™ qPCR Primer for IFNB1(NM_002176.3) Search again
Product ID:
HQP100812
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IFB, IFF, IFN-beta, IFNB
Gene Description:
interferon beta 1
Target Gene Accession:
NM_002176.3(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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Gene References into function
- effect on beta-chemokine expression in differentiating human peripheral blood monocytes
- IRF-3-dependent, NFkappa B- and JNK-independent activation of the 561 and IFN-beta genes in response to double-stranded RNA
- mediates terminal differentiation of human cortical thymic epithelial cells and in particular measles virus-infected cells
- suppresses the proliferations of melanoma cells in an autocrine manner; and is also expressed by melanoma cells and melanocytes
- IFN-beta in combination with TRAIL/Apo2L synergistically induces apoptosis and inhibits melanoma cell proliferation in vitro, at least in part by cleavage of the X-linked inhibitor of apoptosis (XIAP).
- IL-1 functions to limit CMV spread by increasing the expression of IFN-beta, which in turn reduces production of infectious virus.
- Expression profiling and regulation of liver metastases in colorectal cancer cells
- primarily mediates effects on megakaryocytic cells and platelets rather than on thrombopoietin-producing hepatocytes
- IFN-beta inhibits neutrophil apoptosis in a phosphatidylinositol 3-kinase-dependent manner, which requires activation of protein kinase C-delta and induction of NF-kappa B-regulated genes.
- interferon beta has a role in TNFalpha differentially regulating the expression of proinflammatory genes and DNA synthesis
- lipopolysaccharide-TLR4-mediated activation of IFN-beta requires the adapter complex of TICAM-2 and TICAM-1
- Influenza B virus nonstructural protein (NS1)functions as a beta interferon antagonist
- interferon beta synthesis in human macrophages is blocked by oxidized LDL by interfering with IRF3 activation
- Hantaann virus induced the production of beta interferon (IFN-beta) in HUVECS (human umbilical vein endothelial cells), whereas expression of this cytokine was barely detectable in the supernatant or in extracts from Tula virus-infected HUVECs
- suppression of IFN signaling and IFN production by SOC3 occurs during HSV-1 infection
- HSV-1 infection can block the accumulation of IFN-beta triggered by Sendai virus (SeV) infection by blocking the nuclear accumulation of activated IRF-3.
- Expression by cultured bovine BMECs developed as a model of the blood brain barrier.
- The antiviral cytokine interferon beta breaks peripheral tolerance to pancreatic beta cells, influences insulitis progression and contributes to autoimmunity in diabetes and nondiabetes-prone mice.
- type I interferons interact with receptor components results and have roles in the activation of a number of signaling pathways [review]
- Human recombinant IFN-beta induces interleukin (IL)-6 production by U251 astrocytoma cells without induction of IL-1 beta, tumor necrosis factor-alpha and nitric oxide.
- hepatocytes contain two distinct antiviral signaling pathways leading to expression of intereron beta, one dependent upon TLR3 and the other dependent on RIG-I, with little cross-talk between these pathways
- Specific silencing of p53 abrogated the antiviral effect of SD.IFN-beta, suggesting that the tumor suppressor is critically involved in antiviral defense mediated by intracellular IFN.
- demonstrated that inhibition of IFN induction by the HCV NS3/4A protease occurs upstream of the noncanonical IKK-related kinases IKK and TBK-1 & interferes with RIG-I-mediated and TRIF-mediated pathways leading to IRF-3 phosphorylation and activation
- IFN-beta transgene protects against ocular herpes simplex virus type 1 infection in vivo and in vitro via selective up-regulation of the oligoadenylate synthetase (OAS)-1a pathway and by altering protein phosphorylation in antiviral signaling cascades.
- far upstream factor binding sites within the IFN-beta domains of both humans and mice
- Luciferase reporter analyses identified tandem interferon response factor-binding sites in positive regulatory domains I and III of the IFNB promoter as a key target of PKA inhibition.
- human PNPase mRNA upregulation by beta-interferon has no effect on protein level in melanoma cell lines
- mechanism of IFN-beta induction by human cytomegalovirus (HCMV) was investigated; results suggests that PI3-K and/or NF-kappaB may be related with the induction pathway of IFN-beta by HCMV
- A comparison of Sendai virus stocks containing various copyback and internal deletion DI genomes for their ability to activate reporter genes driven by the IFNbeta promoter is presented.
- In vivo induction of ITGA-11 is detected in spleen and lungs of human recombinant IFN-beta treated BALB/c mice.
- Might exert its anti-inflammatory effects mainly by reducing the antigen-presenting capacity of central nervous system-specific antigen-presenting cells, which in turn inhibits the effector functions of encephalitogenic T cells.
- We discuss here the capacity of YY1 to either repress (through histone deacetylase recruitment) or activate (through CBP recruitment) IFN-beta gene expression according to the occupancy of either only its -90 site or both its -122 and -90 sites.
- IPS-1, IRF3, and IFNbeta have critical roles in Legionella infection of lung epithelium
- IFN-beta and a number of IFN-inducible genes were upregulated by transfection of the PTX1-VP22 fusion protein in the prostate cancer cell line PC-3
- The NS1 of influenza A virus binds to RIG-I and inhibits downstream activation of IRF-3, preventing the transcriptional induction of IFN-beta.
- Both the cytoplasmic and TLR3-mediated dsRNA recognition pathways converge upon NAP1 for the activation of the IRF-3 and IFN-beta promoter.
- IFN-beta potently induces endothelial chemokine expression at the transcriptional level
- ability of bICP0 to reduce interferon regulatory factor 3 protein levels is important with respect to disarming the interferon response during productive infection
- Antiviral gene expression in RA, especially due to TLR ligands and TNFalpha, is dependent on IKKepsilon and IRF-3, and this pathway plays a key role in the production of type I IFNs and chemokines such as RANTES.
- Bovine parainfluenza virus type 3 C and V proteins were found to suppress double-stranded RNA-stimulated IFN-beta production.
- structure of IRF-3 DNA binding domain in complex with the complete PRDIII-I regulatory element of the IFN-beta enhancer
- crystallization and modeling of the interferon-beta enhanceosome
- ifn-beta gene activation by K-bZIP is independent of IRF-3 and NF-kappaB activation.
- IFNB1 mRNA levels in virus-infected dendritic cells exhibit cell-to-cell variation.
- depletion of endothelial progenitor cells caused by excessive IFN-I may be linked to endothelial dysfunction and increased cardiovascular risk in systemic lupus erythematosus
- Dermatomyositis and polymyositis are diseases characterized by the systemic overexpression of IFNalpha/beta-inducible genes
- While IFN-beta pretreatment increases slightly the expression of maturation markers in TLR2- or TLR4-stimulated DC, it is able to modulate selectively the secretion of inflammatory and immuno-regulating cytokines.
- The functional association between TLR4 and the S1P1 receptor demonstrates a novel mechanism in the regulation of IFN-beta and CXCL-10 in human primary gingival epithelial cells.
- Our results indicate that rhinovirus type 14 (RV14) infection induces very low levels of IFN-beta mRNA and interfers with IRF-3 activation.
- Retinal pigment epithelial cell induction of IFN-beta during Toll-like receptor signaling in the retina is an immunosuppressive mechanism that limits immunopathologic damage by inhibiting ICAM-1 adhesion molecule synthesis and stopping CXCL9 production.
- These data define the role of the ISGF3 members in IFN-beta inhibitory signaling.
- Activation of HLA-B27 promoter is a sequential event, and that TNF-alpha and IFN-beta are major participants at different timepoints.
- pharmacogenomic analysis of variation in the pharmacological response to IFNbeta between patients
- patients with differing arteriogenic response as measured with collateral flow index display differential transcriptomes of stimulated monocytes; nonresponders show increased expression of IFN-beta and its downstream targets
- TLR3 and 9 as well as IFN-beta and TNF-alpha are expressed in verruca and molluscum contagiosum skin lesions and may play a pivotal role in cutaneous innate immune responses
- PTP1B is a physiological negative regulator of TLR signaling via suppression of both MyD88- and TRIF-dependent production of proinflammatory cytokine and IFN-beta in macrophages.
- This study indicates that the increased type I IFN activity observed in Sjogren's syndrome patients is not only a local but also a systemic phenomenon and points to plasmacytoid dendritic cells as a possible source of this activity.
- Respiratory Syncytial Virus G protein inhibits TLR3/4 mediated interferon beta induction.
- Study reports that stochastic and monoallelic expression of the IFN-B gene depends on interchromosomal associations with 3 identified distinct genetic loci that could mediate binding of the limiting transcription factor NF-kappaB to the IFN-B enhancer.
- These findings indicate that the Hantavirus NY-1V Gn cytoplasmic tail forms a complex with TRAF3 which disrupts the formation of TBK1-TRAF3 complexes and downstream signaling responses required for IFN-beta transcription.
- demonstrates a novel role for Ro52 in turning off and thus limiting IRF3-dependent type I IFN production by targeting the transcription factor for polyubiquitination and subsequent proteasomal degradation
- IFN-beta inhibits IFN-gamma production in general, presumably alleviating the detrimental influence of IFN-gamma in MS.
- In conclusion, intracellular bacteria and cytosolic poly(dA-dT) activate IFNbeta responses in different human cells without requiring human ZBP1.
- aberrant splicing of IRF3 in HCC contributes to the defect in IFN-mediated antiviral defenses.
- Assembly of interferon-beta enhanceosome from its individual protein components and of enhancer DNA has been studied in solution.
- influenza A viruses not only suppress IFNbeta gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the SOCS-3 protein
- Riplet/RNF135 promotes RIG-I-mediated interferon-beta promoter activation
- a novel TLR-independent pathogen-sensing mechanism in immune and nonimmune cells that converges on TBK1 and IFN regulatory factor 3 for activation of IFN-beta gene expression.
- SOCS1-regulation of the IFN beta-dependent component of the LPS-induced TLR4 signaling pathway may contribute to the down-regulation of inflammatory cytokine production
- IFN-beta appears to sensitize neuroblastoma cells to the cytotoxic effects of temozolomide through attenuation of MGMT expression
- These findings reveal a hitherto unknown IFN-beta/SOD1 axis in Leishmania infection