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Validated All-in-One™ qPCR Primer for IRF3(NM_001571.5) Search again
Product ID:
HQP101161
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IIAE7
Gene Description:
interferon regulatory factor 3
Target Gene Accession:
NM_001571.5(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
IRF3 encodes interferon regulatory factor 3, a member of the interferon regulatory transcription factor (IRF) family. IRF3 is found in an inactive cytoplasmic form that upon serine/threonine phosphorylation forms a complex with CREBBP. This complex translocates to the nucleus and activates the transcription of interferons alpha and beta, as well as other interferon-induced genes. [provided by RefSeq].
Gene References into function
- human interferon regulatory factor-3 (IRF-3) gene promoter contains a functional SPH element that is bound by SBF/Staf in vitro and in transfected cells
- Preferential binding sites for interferon regulatory factors 3 and 7 involved in interferon-A gene transcription
- IRF-3 recognizes nucleocapsid structures during measles virus infections and triggers induction of interferon production
- Direct involvement of CREB-binding protein/p300 in sequence-specific DNA binding of virus-activated interferon regulatory factor-3 holocomplex.
- IRF-3-dependent, NFkappa B- and JNK-independent activation of the 561 and IFN-beta genes in response to double-stranded RNA
- IRF3 mediates a TLR3/TLR4-specific antiviral gene program.
- IRF3 binds to p300/CBP and acts as a transcription factor
- Ser(396) within the C-terminal Ser/Thr cluster is targeted in vivo for phosphorylation following virus infection and plays an essential role in IRF-3 activation
- hIRF3 inhibited cell growth, blocked DNA synthesis, and induced apoptosis, while a dominant negative mutant transformed 3T3 cells, implying that IRF3 may function as a tumor suppressor and its dominant negative mutant may have a role in tumorigenesis.
- IKKepsilon and TBK1 have a pivotal role in coordinating the activation of IRF3 and NF-kappaB in the innate immune response.
- In Ebola virus-infected cells, VP35 inhibits the induction of antiviral genes, including the IFN-beta gene, by blocking IRF-3 activation
- Bunyamwera (BUN) NSs protein can delay cell death in the early stages of BUN infection by inhibiting IRF-3-mediated apoptosis.
- LPS-TLR4 signaling to IRF-3/7 and NF-kappaB involves the toll adapters TRAM and TRIF.
- p65 promoted transactivation of gene expression by IRF-3; a dominant negative form of I kappa B kinase 2 and a mutant form of I kappa B, which acts as a super-repressor of NF-kappa B, blocked activation of the ISRE
- Ser-386 is the target of the IRF-3 kinase and critical determinant for the activation of IRF-3
- herpes simplex virus ICP0 blocks interferon regulatory factor IRF3-mediated activation of interferon-stimulated genes; the RING finger domain of ICP0 is essential for this activity
- enveloped particles from RNA and DNA viruses induce interferon-stimulated genes (ISGs) in the absence of IFN production and virus replication through activation of IRF3
- double-stranded RNA-induced TLR3/TRIF-mediated NF-kappaB and IRF3 activation diverge at TRIF
- IRF3 activities are essential for the initiation of transcription of the IFNbeta gene
- activated by West Nile Virus (WNV)infection. Irf-3 target genes function to constrain WNV infection and limit cell-to-cell virus spread.
- Cytomegalovirus pp65 prevents activation of IRF-3, a primary mediator of the type I interferon response.
- NF-kappaB and interferon regulatory factor, the two major transcription factors activated by virus infection, were essential for the induction of two sets of genes by Sendai virus
- activation inhibited by Rabies virus P protein
- ArgII gene is an early IRF-3-regulated gene, which participates in the interferon-independent antiviral response through polyamine production and induction of apoptosis.
- JEV and DEN-2 initiate the host innate immune response through a molecular mechanism involving RIG-I/IRF-3 and PI3K/NF-kappaB signaling pathways
- Expression of IKK-i can activate both NFkappaB and IRF3, leading to the production of several cytokines including interferon beta.
- The present study identified a specific interaction between IRF3 and chaperone heat-shock protein of 90 kDa (Hsp90).In addition, TBK1 is found to be a client protein of Hsp90 in vivo.
- West Nile virus avoids IRF3 pathway through RIG-1 dependent and independent pathways early in infection when it is most sensitive to host cell defenses
- IRF3 induces cell growth inhibition and cellular senescence through activation of p53 tumor suppressor
- belongs to one signaling pathway that mediates induction of gene expression, which, in concert, mediates proliferative activity toward endothelial cells
- HCV infection transiently induces RIG-I- and IPS-1-dependent IRF-3 activation
- Rhinovirus type 14 infection inhibits the host type I interferon in vitro response by interfering with IRF-3 activation.
- expression of the LCMV nucleoprotein (NP) is sufficient to inhibit both IFN production and nuclear translocation of IRF-3
- IPS-1, IRF3, and IFNbeta have critical roles in Legionella infection of lung epithelium
- IRF-3 is a key molecule controlling HCV replication through modulation of host interferon gene responses.
- Transduction of active forms of IRF-3 or IRF-7 differentially modulate the apoptotic and antitumor properties of primary macrophages.
- hypothesized that HSV-1 ICP0 recruits activated IRF-3 & CBP/p300 to nuclear structures, away from host chromatin; this leads to inactivation & accelerated degradation of IRF-3, resulting in reduced transcription of IFN-beta & inhibition of host response
- Both the cytoplasmic and TLR3-mediated dsRNA recognition pathways converge upon NAP1 for the activation of the IRF-3 and IFN-beta promoter.
- ability of bICP0 to reduce IRF3 protein levels is important with respect to disarming the interferon response during productive infection
- proteasome dependent IRF3 degradation in rotavirus infected cells is dependent on the presence of rotavirus NSP1 and the integrity of the N-terminal zinc-binding domain.
- 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.
- expression patterns of IRF3 & IRF7 in normal lymph nodes, reactive hyperplastic lymph nodes & pediatric lymphomas; results suggest IRF3 was activated mainly in histiocytes & T cells under inflammatory conditions but activation was attenuated in lymphoma
- TLR3, PI3K, and IRF3 are involved in the poly IC-induced galectin-9 expression in HUVECs
- analysis of a two-step phosphorylation model for IRF-3 activation mediated by TBK1
- IRF-3 is required for efficient apoptosis following reovirus infection, suggesting a common mechanism of antiviral cytokine induction and activation of the cell death response.
- structure of IRF-3 DNA binding domain in complex with the complete PRDIII-I regulatory element of the IFN-beta enhancer
- Results show that IRF3 signalling is inhibited by YopJ.
- poly(I:C)induction of IDO was mediated in part by IFN-beta but not IFN-gamma, and both NF-kappaB and interferon regulatory factor 3 (IRF3) were required.
- Sin Nombre virus particles initiate a heretofore unrecognized cellular pattern-recognition receptor by engaging a novel IRF3-independent pathway that activates the innate immune response.
- K-bZIP prevents IRF-3 from binding to the IFN-beta promoter and precludes the formation of the enhanceosome, required for maximal ifn-beta gene transcription
- Data suggest that regulation of IRF-3-dependent innate antiviral defenses by papain-like protease may contribute to the establishment of SARS-CoV infection.
- HIV-1 virion-associated accessory proteins Vif and Vpr can independently degrade IRF-3.
- These results indicate that HCV can transiently trigger IRF-3 activation during virus spread and that in chronic HCV, IRF-3 activation within infected hepatocytes occurs but is limited.
- These results demonstrated that IRF-3 controlled the fate of the SeV-infected cells by promoting apoptosis and preventing persistence.
- Polyinosinic-polycytidylic acid and LPS were used to study type-I IFN and TNF responses in human macrophages which activate IRF3 induction.
- Our results indicate that rhinovirus type 14 (RV14) infection interfers with IRF-3 activation.
- The study establishes a molecular link between the role of serine 339 in IRF-3 homodimerization, CBP association, and its destabilization.
- Epstein-Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling.
- These results indicate that Ser386 and Ser396 are critical for IRF-3 activation, and support a phosphorylation-oligomerization model for IRF-3 activation.
- activation and formation of TICAM-1 signalosomes with NF-kappaB and interferon regulatory factor-3 requires oligomerization induced at two different sites and RIP1 binding
- Results show that the promoter single-nucleotide polymorphisms of the IRF3 gene are significantly associated with resistance against systemic lupus erythematosus.
- IRF3-dependent pathway is not essenial for repression of ICPO-null mutant herpes simplex virus type 1 in fibroblasts.
- SUMO modification and RIG-I activation are an integral part of IRF3 and IRF7 activity that contributes to postactivation attenuation of IFN production
- 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
- Study shows that the E3 ubiquitin ligase RBCC protein interacting with PKC1 (RBCK1) catalyzes the ubiquitination and degradation of IRF3.
- MKK4 activates c-Jun and MKK7 activates both c-Jun and IRF3 through JNK-dependent mechanisms.
- aberrant splicing of IRF3 in HCC contributes to the defect in IFN-mediated antiviral defenses
- results suggest MITA is a critical mediator of virus-triggered IRF3 activation and IFN expression and further demonstrate the importance of certain mitochondrial proteins in innate antiviral immunity.
- PKR facilitates the host innate immune response and apoptosis in virus-infected cells by mediating IRF-3 activation through the mitochondrial IPS-1 signal transduction pathway
- 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.
- PKR, in addition to IPS-1 and IRF3 but not TRIF, was required for maximal type I IFN-beta induction and the induction of apoptosis by both transfected PRNAs and polyinosinic-polycytidylic acid.
- Abundance of IRF-3 protein is a determinant in the polyinosinic:polycytidylic acid-mediated antiviral signalling pathway.
- IRF3 and p38 MAP kinase separately and predominantly contribute to avian influenza A virus H5N1-mediated induction of interferon (IFN)-beta, IFN-lambda 1 and monocyte chemoattractant protein-1 but only partly control tumor necrosis factor-alpha induction
- Altogether, these data further highlight the respective functions of IRF-3 and IRF-7 to program apoptotic, immune and anti-tumor responses.
- carbon monoxide treatment inhibits dendritic cell immunogenicity induced by TLR ligands and that blockade of IFN regulatory factor 3 is associated with this effect
- Neither of the mitogen-activated protein kinases ERK1/2, JNK, or p38 nor the transcription factor interferon regulatory factor 3 were involved in the direct transactivation of HIV-LTR through stimulation of TLR4.