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the state of type I IFN induction and response to, in SAMHD1 knockout (KO) human monocytic cells, was examined.
Authors show that the transcription factor ThPOK binds cooperatively with NF-kappaB to NRCs and mediates their physical proximity with the IFNB1 gene via its ability to oligomerize when bound to DNA.
hypoxia triggers the production of IFN-I in vitro, and may contribute to the pathogenesis of dermatomyositis together with other inflammatory factors.
These results indicate that human dendritic cells activated by Lactic acid bacteria enhance Th1 immunity depending on IFN-beta secretion in response to bacterial Double-Stranded RNA.
Here, the authors identified multiple RNA regions in Kaposi's sarcoma-associated herpesvirus as potential virus ligands that bind to RIG-I and stimulate RIG-I-dependent but RNA Pol III-independent IFN-beta signaling.
Data indicate a mechanism used by monocyte chemotactic protein-inducing protein 1 (MCPIP1) to negatively regulated type I IFN interferon-beta antiviral defense.
It has been shown that HCMV has evolved mutational robustness against IFN-beta by limiting the presence of APOBEC3G hot spots in essential open reading frames of its genome.
These experimental data establish the retromer complex as a key spatiotemporal regulator of IFNAR endosomal sorting and a new factor in type-I IFN-induced JAK/STAT signalling and gene transcription.
RIG-I-like receptors have a role in induction of interferon-beta1 in antiviral gene expression
Transcriptomic analysis of early untreated dermatomyositis muscles revealed that the main cluster of down-regulated genes was mitochondria-related. Histochemical, electron microscopy, and in situ oxygraphy analysis showed mitochondrial abnormalities, including increased reactive oxygen species (ROS) production and decreased respiration, which was correlated with low exercise capacities and a type I IFN signature.
Gas6 bound to the fiber proteins of adenovirus and suppressed IFN beta production.
The overexpression of NPIPB3 restored the interferon-beta responses in severe acute respiratory syndrome coronavirus open reading frame 6 (SARS-CoV ORF6) expressing cells, indicating that the interaction of SARS CoV ORF6 and NPIPB3 reduced Type I interferon antagonism by SARS-CoV ORF6.
The results demonstrate that cystatin B interferes with the STAT-1 signaling and IFN-beta-antiviral responses perpetuating HIV in macrophage reservoirs.
The review focuses on the value of the type I and III interferon subtypes (alphas, beta and lambdas) as therapeutics for prevention and treatment of viral infections (influenza, herpes, human immunodeficiency virus and hepatitis viruses).
This review briefly discusses the dysregulation of main T cell subpopulations in CNS autoimmunity and summarized the T cell targeted effects of endogenous and exogenous IFN-beta in health and EAE/MS, with emphasis on the direct actions of IFN-beta on each T cell subset involved in the disease.
c-Cbl negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 ubiquitination and degradation.
YPEL5 silencing enhanced the induction of IFNB1 by pattern recognition receptors and phosphorylation of TBK1/IKBKE kinases, whereas co-immunoprecipitation experiments revealed that YPEL5 interacted physically with IKBKE.
The effect of topical TREX1 knockdown and local interferon production on HIV transmission in human cervicovaginal explants and humanized mice, is reported.
The current knowledge on IFNbeta from its structure, dynamic conformation, signaling pathway, and mechanism of action to its therapeutic effects is summarized.
this study shows that the IFN-beta/STAT1 pathway is dysregulated in inflammatory bowel disease
The authors provide evidence that IFIT2 increases the pathological effects of invasive Candida albicans and that administration of interferon-beta has deleterious effects during infection.
The expression levels of miR-182, PKR, and IFN-beta are altered in rheumatoid arthritis (RA) and are significantly correlated with the osteoclastogenic capacity of RA monocytes.
IFNbeta activates neuronal PI3K/Akt signalling and Akt binds to transcription factor FoxA1 that translocates to the nucleus and induces PDL1. Conversely, inhibition of PI3K/Akt, FoxA1 and PDL1 blocked neuronal ability to generate FoxA1(+)Tregs.
Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNbeta, which induced beta-cell apoptosis by increasing the expression of Xaf1.
Reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) prevented mitochondrial dysfunctions, type I IFN-stimulated transcript levels, inflammatory cell infiltrate, and muscle weakness in an experimental autoimmune myositis mouse model. Thus, these data highlight a central role of mitochondria and ROS in dermatomyositis .
Nontypeable Haemophilus influenzae DNA as a Pathogen-Associated Molecular Pattern Molecules triggered I-IFN response, which was STING/TBK1/IRF3 dependent.
The Lipopolysaccharide and IFN-beta-mediated increase of STAT1 mRNA and protein levels was abrogated by chelation of Zn(2+) with the membrane permeable chelator N,N,N',N'-Tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) in RAW 264.7 macrophages.
MAVS is essential for spontaneous high basal expression of IFN-beta in cardiac myocytes and the heart.
Mycobacterium smegmatis induces higher Ifnb expression in macrophages than Mycobacterium avium subspecies.
Chronic presence of IFN-I in the brain microenvironment, which negatively affects cognitive function, is mediated via modulation of microglial activity.
In experimental autoimmune encephalomyelitis, IFN-beta inhibited downstream inflammatory cytokines through the inhibition of PI3K/AKT/NF-kappaB axis and p38, JNK-MAPK, as well as the regulation of mTOR complexes. Moreover, IFN-beta inhibited Th17 differentiation and influenced the acetylation of the Il17a and Opn gene promoters. IFN-beta plays a role in Th17 differentiation partly through the inhibition of OPN.
Rb selectively inhibits innate IFN-beta production by enhancing deacetylation of Ifnb1 promoter, exhibiting a previous unknown non-classical role in innate immunity, which also suggests a role of Rb in the regulation of type I IFN production in inflammatory or autoimmune diseases.
The TBK1 Y179A mutant failed to rescue type I IFN production by virally infected RAW264.7 macrophages deficient in TBK1.
this study shows that poly I:C treated PAR-1-/- mice given the thrombin inhibitor dabigatran etexilate exhibited less IFNbeta and CXCL10 expression in the spleen and plasma
The data demonstrate that an atypical TLR7 signaling pathway contributes to type interferon-beta expression during Y. pestis infection and suggest that the TLR7-driven type I IFN response plays an important role in determining the outcome of plague.
Long-term exposure to atmospheric particulates, PM2.5 up-regulated H3K4 and H3K9 methylation in IL-6 and IFN-beta promoter regions through down-regulating Kdm6a expression. The results suggest that short-term exposure to PM2.5 significantly enhances the survival rate of influenza A-contaminated mice, while long-term PM2.5 inhalation lowers the capacity of pulmonary macrophages to secrete IL-6 and IFN-beta.
Extracellular ATP reduces the replication of VSV, Newcastle disease virus, murine leukemia virus and HSV in vivo and in vitro through the P2X7 receptor; ATP increases IFN-beta expression. Mechanistically, ATP facilitates IFN-beta secretion through P38/JNK/ATF-2 signaling pathways, which are crucial in promoting antiviral immunity.
BVDV2-E significantly increased IFN-beta activity compared to BVDV2-wt.
The data confirm the involvement of EHMT2 in the epigenetic regulation of IFN-b and demonstrate the activation of a general antiviral state after EHMT2 inhibition.
The authors provide evidence that ICP27 protein encoded by bovine herpesvirus type 1, a viral early protein that shuttles between the nucleus and cytoplasm inhibits transcriptional activity of two bovine IFN-beta gene promoters (IFN-beta1 and IFN-beta3).
The authors demonstrate that bovine herpesvirus 1 bICP0 effectively inhibits bovine IFN-beta promoter activity and induces IRF3 degradation.
These studies provide evidence that virus infection differentially stimulates expression of the three bovine IFN-beta genes.
recombinant bovine respiratory syncytial virus lacking the NS proteins, and those lacking NS2 in particular, are strong inducers of IFN-alpha/beta in bovine nasal fibroblasts and bronchoalveolar macrophages.
PorcineCircoVirus2 infection activates the cGAS/STING signaling pathway to induce IFN-beta production and the knockdown of cGAS and STING decreases viral replication in PK-15 cells
Results demonstrated that p53 may mediate IFN-beta signaling to inhibit viral replication early after Transmissible gastroenteritis virus infection.
Key regulators involved in Porcine circovirus 2 infection were identified as IFNbeta, DDX58 (RIG-I), and IRF7.
These results indicate that porcine circovirus type 2 disrupts the interaction of KPNA3 with p-IRF3 and blocks p-IRF3 translocation to the nucleus, thereby inhibiting IFN-beta induction in PK-15 cells.
Nuclear export of NSP1alpha of porcine reproductive and respiratory syndrome virus was necessary for its ability for IFN beta inhibition.
Porcine deltacoronavirus nsp5, the 3C-like protease, inhibits interferon-beta production through the cleavage of NEMO.
demonstrated that PRRSV does induce variably, the expression of bioactive IFNbeta protein in the natural host cell.
Highly pathogenic Porcine reproductive and respiratory syndrome virus modulates Interferon-beta expression mainly through attenuating IRF-3 phosphorylation.
Porcine epidemic diarrhea virus nsp1 inhibited the IFN-beta and IRF3 promoter activities.
poIFIT3 plays a significant role in the clearance of swine influenza virus in pigs and potentiates IFN-beta production.
DDX41 is involved in the dsDNA- and dsDNA-virus-mediated type IFN-beta signaling pathway in porcine kidney cells.
VIral NS4 protein antagonizes beta interferon expression by targeting the NF-kappaB essential modulator.
Swine IFN-beta promotes genetic mutation of porcine reproductive and respiratory syndrome virus.
Expression of LSm14A in HEK293 or Marc-145 cells enhanced activities of IFN-beta and NF-kappaB promoters, induced IFN-beta transcription, and potentiated IFN-beta promoter activation, indicating that LSm14A is a potential signal molecule in the IFN-beta pathway.
Overall, data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-alpha/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.
rPoIFN-beta could effectively inhibit the replication of PrV in MDBK cells, especially during the early phage of the virus replication.
either JC1 or DS1 C/EBP site is sufficient to mediate IFN beta-induced down-regulation of SIV long terminal repeat activity and virus replication in macrophages
Hepatitis A virus protein 2B suppresses beta interferon (IFN) gene transcription by interfering with IFN regulatory factor 3 activation.
suppresses the growth of rat glioma cells
, fibroblast interferon
, interferon beta
, interferon, beta 1
, interferon beta-1
, interferon beta 1
, interferon, beta 1, fibroblast