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Human Monoclonal IRF3 Primary Antibody für Inhibition, IF - ABIN967285
Au, Moore, Lowther, Juang, Pitha: Identification of a member of the interferon regulatory factor family that binds to the interferon-stimulated response element and activates expression of interferon-induced genes. in Proceedings of the National Academy of Sciences of the United States of America 1996
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Mouse (Murine) Polyclonal IRF3 Primary Antibody für WB - ABIN1881465
Marichal, Bedoret, Mesnil, Pichavant, Goriely, Trottein, Cataldo, Goldman, Lekeux, Bureau, Desmet: Interferon response factor 3 is essential for house dust mite-induced airway allergy. in The Journal of allergy and clinical immunology 2010
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Human Polyclonal IRF3 Primary Antibody für IHC, ELISA - ABIN1002558
Malmgaard: Induction and regulation of IFNs during viral infections. in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 2004
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Human Polyclonal IRF3 Primary Antibody für ICC, ELISA - ABIN1002559
Fitzgerald, McWhirter, Faia, Rowe, Latz, Golenbock, Coyle, Liao, Maniatis: IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway. in Nature immunology 2003
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Human Polyclonal IRF3 Primary Antibody für IF (cc), IF (p) - ABIN742688
Menasria, Boivin, Lebel, Piret, Gosselin, Boivin: Both TRIF and IPS-1 Adaptor Proteins Contribute to the Cerebral Innate Immune Response against Herpes Simplex Virus 1 Infection. in Journal of virology 2013
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Human Polyclonal IRF3 Primary Antibody für ICC, WB - ABIN6673836
Zhang, Wang, Zhong, Luo, Shang, Liu, Chen, Fang, Xiao: Ubiquitin-specific Protease 15 Negatively Regulates Virus-induced Type I Interferon Signaling via Catalytically-dependent and -independent Mechanisms. in Scientific reports 2016
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Human Polyclonal IRF3 Primary Antibody für IF, IHC - ABIN6674088
Zhu, Wang, Pei, Wang, Wu, Qiu, Zhang, Lv, Li, Zhang: Neddylation controls basal MKK7 kinase activity in breast cancer cells. in Oncogene 2017
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Human Polyclonal IRF3 Primary Antibody für IF, IHC - ABIN6682130
Ye, Chen, Li, Zhao, He, Zohaib, Song, Deng, Zhang, Chen, Cao: Japanese Encephalitis Virus NS5 Inhibits Type I Interferon (IFN) Production by Blocking the Nuclear Translocation of IFN Regulatory Factor 3 and NF-κB. in Journal of virology 2017
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Following spring viremia of carp virus infection, DrIFNPhi1/3 and DrIRF1/3/7 transcripts are significantly induced in zebrafish tissues, which correlates with the replication of spring viremia of carp virus. data provide evidence that fish and mammals have evolved a similar IRF-dependent regulatory mechanism fine-tuning IFN gene activation.
Interferon regulatory factor (IRF)10 inhibits the expression of IFN1 and IFN3 to avoid an excessive immune response, a unique regulation mechanism of the IFN responses in lower vertebrates.
Hepatitis A virus protein 2B suppresses beta interferon (IFN) gene transcription by interfering with IFN regulatory factor 3 activation.
MyD88 interacts with interferon regulatory factor (IRF) 3 and IRF7 in Atlantic salmon (Salmo salar)
Reduced GATA-1 could be responsible for the upregulation of IRF-3 in lung adenocarcinoma cells through binding with a specific domain of IRF-3 promoter.
STING-IRF3 pathway promotes hepatocyte injury and dysfunction by inducing inflammation and apoptosis and by disturbing glucose and lipid metabolism.
beta-catenin interacted with IRF3 and blocked its nuclear translocation.
Upregulation of endogenous SAMHD1 expression is attributed to the phosphorylation and nuclear translocation of IRF3.
In this work, the authors found that differences in type 1 interferon production by T1 and T3 reoviruses correlate with differential IRF3 activation.
Proteins 8b and 8ab of severe acute respiratory syndrome coronavirus physically interact with IRF3 and in induced degradation of IRF3 in a ubiquitin-proteasome-dependent manner.
Our results highlight the importance of IRF3 and type-I IFNs signaling for the pro-apoptotic effects induced by RA and synthetic dsRNA in breast cancer cells.
In the current study, we studied the role of MITA (Mediator of IRF3 Activation), a regulator of innate immunity, in the regulation of autophagy and its implication in cell death of breast cancer cells. Here, we report that MITA inhibits the fusion of autophagosome with lysosome as evident from different autophagy flux assays
New research suggests that altering a subset of extracellular matrix factors, including interferon regulatory factor (IRF)3 and casein kinase (CK)2, may decrease the migratory potential of these aggressive tumors.
IRF-3 gene polymorphisms were associated with the susceptibility and prognosis of CLL, it can be used as an auxiliary index for clinical detection of CLL.
Clarithromycin acts a crucial modulator of the innate immune response, particularly IFN production, by modulating IRF-3 dimerization and subsequent translocation to the nucleus of airway epithelial cells.
c-Cbl negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 ubiquitination and degradation.
data describe an unappreciated role for EAP30 in IRF3-dependent innate antiviral response in the nucleus.
IRF-3 is an important regulator of ORMDL3 induction following RSV infection by binding directly to the promoter of ORMDL3
above findings suggest that ATG5-ATG12 positively regulate anti-viral NF-kappaB and IRF3 signaling during FMDV infection, thereby limiting FMDV proliferation. FMDV has evolved mechanisms to counteract the antiviral function of ATG5-ATG12, via degradation of them by viral protein 3C(pro).
NEMO-IKKbeta Are Essential for IRF3 and NF-kappaB Activation in the cGAS-STING Pathway
these data suggest that HNSs, an antagonist of host innate immunity, interacts with TBK1 and thereby hinders the association of TBK1 with its substrate IRF3, thus blocking IRF3 activation and transcriptional induction of the cellular antiviral responses.
our data provide an important insight into STING-mediated induction of type I and III IFNs and subsequent antiviral signaling pathways that regulate VZV replication in human dermal cells.
IRF3 is a major transcriptional regulator of adipose inflammation and is involved in maintaining systemic glucose and energy homeostasis
this study shows that IRF-3-mediated apoptosis of virus-infected cells could be an effective antiviral mechanism, without expression of the interferon-stimulated genes
The authors used recombinant classical swine fever virus N(pro) and swine IRF3 proteins and show that N(pro) interacts with IRF3 directly without additional proteins and forms a soluble 1:1 complex.
Amino acid residues in the N-terminal domain of Npro are involved in the stability of Npro, in interaction of Npro with IRF-3 and subsequent degradation of IRF-3, leading to downregulation of IFN-alpha/beta production.
The obtained results showed that PRRSV nsp1 could inhibit Poly(I:C)-induced IFN-beta promoter activity in MARC-145 cells by down-regulating the protein level of IRF-3 and inhibiting the phosphorylation of IRF-3.
proteasomal degradation of IRF3 is induced by a direct or indirect interaction with N(pro).
we revealed roles for IRF3 in balancing Th1- and T follicular helper-dependent immunity during nonlethal infection with blood-stage Plasmodium parasites
this study shows that activation of IRF3 contributes to IFN-gamma and ISG54 expression during the immune responses to B16F10 tumor growth
IRF3 exacerbates P. aeruginosa-induced mortality in mice by inhibiting neutrophil adhesion and recruitment to the lungs
IRF3 expression and activation depend on the signal transduction of the the urotensin II/urotensin receptor (UII/UT) system, and play important roles in UII/UT
Interruption of IRF3-dependent signaling resulted in decreased cardiac expression of inflammatory cytokines and chemokines and decreased inflammatory cell infiltration of the heart, as well as in attenuated ventricular dilation and improved cardiac function.
This study reveals a critical role of NSD3-mediated IRF3 methylation in enhancing antiviral innate immunity.
these results suggested that the basal promoter activity of the mIRF-3 gene is regulated by transcription factors Egr2 and YY1 in NIH3T3 cells
Data show that stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI)-associated STING N153S mutation triggers IRF3-independent immune cell dysregulation and lung disease in mice.
study provided evidence that the ability of ICP34.5 to control IRF3 activation is through its ability to reverse translational shutoff and sustain the expression of other IFN inhibitors encoded by the virus
This study did not find non-conservative mutations among SJL, B10.S, B6 and B10 mice in the IRF3 amino acid sequence, and show SJL bone marrow-derived macrophages infected with Theiler's murine encephalomyelitis virus exhibit increased virus RNA replication and infectious virus yields as well as greater IL-6 production than C57Bl strain (including B10.S) cultures.
The IRF-3 pathway is essential for tick-borne encephalitis virus-induced RANTES production in the brain.
Yersinia YopJ negatively regulates IRF3-mediated antibacterial response through disruption of STING-mediated cytosolic DNA signaling.
Findings indicate that STING-TBK1-IRF3 pathway mediates a crosstalk between ER stress and apoptosis during M. bovis infection, which can effectively control intracellular bacteria.
GPR146 has an antiviral role in fighting against viral infection, although the GPR146-mediated protection is eliminated by IRF3/HES1-signalling.
Results establish Irf3, known mostly for its role in antiviral responses, as a transcription factor involved in the induction of Th2 responses through the promotion of pro-Th2 costimulation in CD11b(+) dendritic cells
Rubicon specifically interacts with the interferon regulatory factor (IRF) association domain (IAD) of IRF3, and this interaction leads to inhibition of the dimerization of IRF3, which negatively regulates interferon-mediated antiviral response.
These results link the stimulation of the innate immune response observed in 3 NCR-transfected cells to the intracellular type I IFN signaling pathway and suggest the potential use of these molecules for antiviral strategies in cattle.
The authors demonstrate that bovine herpesvirus 1 bICP0 effectively inhibits bovine IFN-beta promoter activity and induces IRF3 degradation.
cpBVDV infection causes a marked loss of interferon regulatory factor 3 (IRF-3), a cellular transcription factor that controls interferon synthesis.
This gene encodes a member of the interferon regulatory transcription factor (IRF) family. The encoded protein 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. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
interferon regulatory factor 3
, interferon regulatory factor 3-like