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抗Human IFNB1 抗体:
抗Mouse (Murine) IFNB1 抗体:
抗Rat (Rattus) IFNB1 抗体:
Human Polyclonal IFNB1 Primary Antibody for ELISA, ICC - ABIN4321105
Colonna: TLR pathways and IFN-regulatory factors: to each its own. in European journal of immunology 2007
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Human Polyclonal IFNB1 Primary Antibody for IHC, ELISA - ABIN1002472
Gresser: Wherefore interferon? in Journal of leukocyte biology 1997
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Chicken Polyclonal IFNB1 Primary Antibody for Func, IP - ABIN2474124
Sick, Schultz, Staeheli: A family of genes coding for two serologically distinct chicken interferons. in The Journal of biological chemistry 1996
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Rat (Rattus) Polyclonal IFNB1 Primary Antibody for ELISA, WB - ABIN285821
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. in Physiology & behavior 2008
Human Polyclonal IFNB1 Primary Antibody for 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. in Journal of leukocyte biology 2016
Human Monoclonal IFNB1 Primary Antibody for 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. in Japanese circulation journal 1990
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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 (显示 CSTB 抗体) interferes with the STAT-1 (显示 STAT1 抗体) signaling and IFN-beta-antiviral responses perpetuating HIV in macrophage reservoirs.
The review focuses on the value of the type I and III interferon (显示 IFNA 抗体) 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 (显示 CBL 抗体) negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 (显示 IRF3 抗体) ubiquitination and degradation.
YPEL5 silencing enhanced the induction of IFNB1 by pattern recognition receptors and phosphorylation of TBK1 (显示 TBK1 抗体)/IKBKE (显示 IKBKE 抗体) kinases, whereas co-immunoprecipitation experiments revealed that YPEL5 interacted physically with IKBKE (显示 IKBKE 抗体).
The effect of topical TREX1 (显示 TREX1 抗体) knockdown and local interferon (显示 IFNA 抗体) production on HIV transmission in human cervicovaginal explants and humanized mice, is reported.
this study shows that the IFN-beta/STAT1 (显示 STAT1 抗体) pathway is dysregulated in inflammatory bowel disease
results demonstrate that Sphingosine 1-phosphate lyase (SPL (显示 SGPL1 抗体)) is a host factor that augments type I IFN responses during influenza A virus infection; study delineates the relationship between IKKepsilon (显示 IKBKE 抗体) and SPL (显示 SGPL1 抗体), which provides a mechanistic understanding of the pro-IFN activity of SPL (显示 SGPL1 抗体)
results suggest that, in addition to its well-known signaling activity, IFN-beta may be directly antimicrobial and be part of a growing family of cytokines and chemokines, called kinocidins, that also have antimicrobial properties.
In experimental autoimmune encephalomyelitis, IFN-beta inhibited downstream inflammatory cytokines through the inhibition of PI3K/AKT (显示 AKT1 抗体)/NF-kappaB (显示 NFKB1 抗体) axis and p38 (显示 CRK 抗体), JNK (显示 MAPK8 抗体)-MAPK (显示 MAPK1 抗体), as well as the regulation of mTOR (显示 FRAP1 抗体) complexes. Moreover, IFN-beta inhibited Th17 differentiation and influenced the acetylation of the Il17a (显示 IL17A 抗体) and Opn (显示 SPP1 抗体) gene promoters. IFN-beta plays a role in Th17 differentiation partly through the inhibition of OPN (显示 SPP1 抗体).
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 (显示 TBK1 抗体) Y179A mutant failed to rescue type I IFN production by virally infected RAW264.7 macrophages deficient in TBK1 (显示 TBK1 抗体).
this study shows that poly I:C treated PAR-1 (显示 MARK2 抗体)-/- mice given the thrombin (显示 F2 抗体) inhibitor dabigatran etexilate exhibited less IFNbeta and CXCL10 (显示 CXCL10 抗体) expression in the spleen and plasma
The data demonstrate that an atypical TLR7 (显示 TLR7 抗体) signaling pathway contributes to type interferon-beta expression during Y. pestis infection and suggest that the TLR7 (显示 TLR7 抗体)-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 (显示 IL6 抗体) and IFN-beta promoter regions through down-regulating Kdm6a (显示 KDM6A 抗体) 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 (显示 IL6 抗体) 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 (显示 P2RX7 抗体); ATP increases IFN-beta expression. Mechanistically, ATP facilitates IFN-beta secretion through P38 (显示 CRK 抗体)/JNK (显示 MAPK8 抗体)/ATF-2 (显示 ATF2 抗体) 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 (显示 EHMT2 抗体) in the epigenetic regulation of IFN-b and demonstrate the activation of a general antiviral state after EHMT2 (显示 EHMT2 抗体) 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 (显示 IRF3 抗体) 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 (显示 IFNA 抗体)/beta in bovine nasal fibroblasts and bronchoalveolar macrophages.
Nuclear export of NSP1alpha of porcine reproductive and respiratory syndrome virus was necessary for its ability for IFN beta inhibition.
Porcine deltacoronavirus nsp5 (显示 SPECC1 抗体), the 3C-like protease, inhibits interferon-beta production through the cleavage of NEMO (显示 IKBKG 抗体).
Highly pathogenic Porcine reproductive and respiratory syndrome virus modulates Interferon-beta expression mainly through attenuating IRF-3 (显示 IRF3 抗体) phosphorylation.
Porcine epidemic diarrhea virus nsp1 inhibited the IFN-beta and IRF3 (显示 IRF3 抗体) promoter activities.
poIFIT3 plays a significant role in the clearance of swine influenza virus in pigs and potentiates IFN-beta production.
DDX41 (显示 DDX41 抗体) is involved in the dsDNA- and dsDNA-virus-mediated type IFN-beta signaling pathway in porcine kidney cells.
VIral NS4 (显示 SOS1 抗体) protein antagonizes beta interferon (显示 IFNA 抗体) expression by targeting the NF-kappaB (显示 NFKB1 抗体) essential modulator.
Swine IFN-beta promotes genetic mutation of porcine reproductive and respiratory syndrome virus.
Expression of LSm14A (显示 LSM14A 抗体) in HEK293 or Marc (显示 CCL7 抗体)-145 cells enhanced activities of IFN-beta and NF-kappaB (显示 NFKB1 抗体) promoters, induced IFN-beta transcription, and potentiated IFN-beta promoter activation, indicating that LSm14A (显示 LSM14A 抗体) is a potential signal molecule (显示 WNT4 抗体) in the IFN-beta pathway.
Overall, data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-alpha (显示 IFNA 抗体)/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha (显示 IFNA 抗体) in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.
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 (显示 IFNA 抗体) (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 type B
, interferon, beta 1, fibroblast
, IFN-alpha/beta receptor 2
, interferon alpha/beta receptor 2
, interferon, beta; receptor
, interferon-alpha/beta receptor 2
, interferon-alpha/beta receptor beta chain
, type I interferon receptor 2