Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human IFNB1 Anticorps:
anti-Mouse (Murine) IFNB1 Anticorps:
anti-Rat (Rattus) IFNB1 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal IFNB1 Primary Antibody pour ELISA, ICC - ABIN4321105
Colonna: TLR pathways and IFN-regulatory factors: to each its own. dans European journal of immunology 2007
Show all 4 Pubmed References
Human Polyclonal IFNB1 Primary Antibody pour IHC, ELISA - ABIN1002472
Gresser: Wherefore interferon? dans Journal of leukocyte biology 1997
Show all 2 Pubmed References
Chicken Polyclonal IFNB1 Primary Antibody pour Func, IP - ABIN2474124
Sick, Schultz, Staeheli: A family of genes coding for two serologically distinct chicken interferons. dans The Journal of biological chemistry 1996
Show all 3 Pubmed References
Human Polyclonal IFNB1 Primary Antibody pour IF (p), IHC (p) - ABIN728158
Quek, Luff, Cheung, Kozlov, Gatei, Lee, Bellingham, Noakes, Lim, Barnett, Dingwall, Wolvetang, Mashimo, Roberts, Lavin: Rats with a missense mutation in Atm display neuroinflammation and neurodegeneration subsequent to accumulation of cytosolic DNA following unrepaired DNA damage. dans Journal of leukocyte biology 2016
Human Polyclonal IFNB1 Primary Antibody pour IP, IHC - ABIN285830
Matsumoto, Takahashi, Shiva, Kawanishi, Kremenik, Kato, Yano: The reduction of voluntary physical activity after poly I:C injection is independent of the effect of poly I:C-induced interferon-beta in mice. dans Physiology & behavior 2008
Human Monoclonal IFNB1 Primary Antibody pour ELISA - ABIN2474122
Horie, Miyazaki, Nonogi, Takizawa, Nagao, Nishida, Kubota, Kawai: Kinetic analyses of creatine kinase release patterns in patients with acute myocardial infarction undergoing emergency coronary arteriography. dans Japanese circulation journal 1990
Show all 2 Pubmed References
It has been shown that HCMV has evolved mutational robustness against IFN-beta by limiting the presence of APOBEC3G (Montrer APOBEC3G Anticorps) hot spots in essential open reading frames of its genome.
These experimental data establish the retromer complex as a key spatiotemporal regulator of IFNAR (Montrer IFNAR1 Anticorps) endosomal sorting and a new factor in type-I IFN-induced JAK (Montrer JAK3 Anticorps)/STAT (Montrer STAT1 Anticorps) signalling and gene transcription.
RIG-I-like receptors have a role in induction of interferon-beta1 in antiviral gene expression
Transcriptomic analysis of e (Montrer ROS1 Anticorps)arly untreated dermatomyositis mus (Montrer NLRP1 Anticorps)cles 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) productio (Montrer ROS1 Anticorps)n and decreased respiration, which was correlated with low exercise capacities and a type I IFN signature.
Gas6 (Montrer GAS6 Anticorps) 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 (Montrer CSTB Anticorps) interferes with the STAT-1 (Montrer STAT1 Anticorps) 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 (Montrer CBL Anticorps) negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 (Montrer IRF3 Anticorps) ubiquitination and degradation.
IFNbeta activates neuronal PI3K/Akt (Montrer AKT1 Anticorps) signalling and Akt (Montrer AKT1 Anticorps) binds to transcription factor FoxA1 (Montrer FOXA1 Anticorps) that translocates to the nucleus and induces PDL1 (Montrer CD274 Anticorps). Conversely, inhibition of PI3K/Akt (Montrer AKT1 Anticorps), FoxA1 (Montrer FOXA1 Anticorps) and PDL1 (Montrer CD274 Anticorps) blocked neuronal ability to generate FoxA1 (Montrer FOXA1 Anticorps)(+)Tregs.
Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNbeta, which induced beta-cell apoptosis by increasing the expression of Xaf1 (Montrer XAF1 Anticorps).
Reactive oxygen species (ROS (Montrer ROS1 Anticorps)) scavenger N-acetyl cysteine (NAC (Montrer NLRP1 Anticorps)) 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 (Montrer ROS1 Anticorps) in dermatomyositis .
Nontypeable Haemophilus influenzae DNA as a Pathogen-Associated Molecular Pattern Molecules triggered I-IFN response, which was STING/TBK1 (Montrer TBK1 Anticorps)/IRF3 (Montrer IRF3 Anticorps) dependent.
The Lipopolysaccharide and IFN-beta-mediated increase of STAT1 (Montrer STAT1 Anticorps) 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 (Montrer MAVS Anticorps) 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.
In experimental autoimmune encephalomyelitis, IFN-beta inhibited downstream inflammatory cytokines through the inhibition of PI3K/AKT (Montrer AKT1 Anticorps)/NF-kappaB (Montrer NFKB1 Anticorps) axis and p38 (Montrer CRK Anticorps), JNK (Montrer MAPK8 Anticorps)-MAPK (Montrer MAPK1 Anticorps), as well as the regulation of mTOR (Montrer FRAP1 Anticorps) complexes. Moreover, IFN-beta inhibited Th17 differentiation and influenced the acetylation of the Il17a (Montrer IL17A Anticorps) and Opn (Montrer SPP1 Anticorps) gene promoters. IFN-beta plays a role in Th17 differentiation partly through the inhibition of OPN (Montrer SPP1 Anticorps).
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.
BVDV2-E significantly increased IFN-beta activity compared to BVDV2-wt.
The data confirm the involvement of EHMT2 (Montrer EHMT2 Anticorps) in the epigenetic regulation of IFN-b and demonstrate the activation of a general antiviral state after EHMT2 (Montrer EHMT2 Anticorps) 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 (Montrer IRF3 Anticorps) 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.
Key regulators involved in Porcine circovirus 2 infection were identified as IFNbeta, DDX58 (RIG-I (Montrer DDX58 Anticorps)), and IRF7 (Montrer IRF7 Anticorps).
These results indicate that porcine circovirus type 2 disrupts the interaction of KPNA3 (Montrer KPNA3 Anticorps) with p-IRF3 (Montrer IRF3 Anticorps) and blocks p-IRF3 (Montrer IRF3 Anticorps) 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 (Montrer SPECC1 Anticorps), the 3C-like protease, inhibits interferon-beta production through the cleavage of NEMO (Montrer IKBKG Anticorps).
Highly pathogenic Porcine reproductive and respiratory syndrome virus modulates Interferon-beta expression mainly through attenuating IRF-3 (Montrer IRF3 Anticorps) phosphorylation.
Porcine epidemic diarrhea virus nsp1 inhibited the IFN-beta and IRF3 (Montrer IRF3 Anticorps) promoter activities.
poIFIT3 plays a significant role in the clearance of swine influenza virus in pigs and potentiates IFN-beta production.
DDX41 (Montrer DDX41 Anticorps) is involved in the dsDNA- and dsDNA-virus-mediated type IFN-beta signaling pathway in porcine kidney cells.
VIral NS4 (Montrer SOS1 Anticorps) protein antagonizes beta interferon expression by targeting the NF-kappaB (Montrer NFKB1 Anticorps) essential modulator.
Swine IFN-beta promotes genetic mutation of porcine reproductive and respiratory syndrome virus.
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