IFNB1 蛋白 (IFNB1)产品概述

Human Interferon, beta 1, Fibroblast (IFNB1) interaction partners

1. It has been shown that HCMV has evolved mutational robustness against IFN-beta by limiting the presence of APOBEC3G (显示 APOBEC3G 蛋白) hot spots in essential open reading frames of its genome.

2. These experimental data establish the retromer complex as a key spatiotemporal regulator of IFNAR (显示 IFNAR1 蛋白) endosomal sorting and a new factor in type-I IFN-induced JAK (显示 JAK3 蛋白)/STAT (显示 STAT1 蛋白) signalling and gene transcription.

3. RIG-I (显示 DDX58 蛋白)-like receptors have a role in induction of interferon (显示 IFNA 蛋白)-beta1 in antiviral gene expression

4. Transcriptomic analysis of e (显示 ROS1 蛋白)arly 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) productio (显示 ROS1 蛋白)n and decreased respiration, which was correlated with low exercise capacities and a type I IFN signature.

5. Gas6 (显示 GAS6 蛋白) bound to the fiber proteins of adenovirus and suppressed IFN beta production.

6. 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.

7. The results demonstrate that cystatin B (显示 CSTB 蛋白) interferes with the STAT-1 (显示 STAT1 蛋白) signaling and IFN-beta-antiviral responses perpetuating HIV in macrophage reservoirs.

8. The review focuses on the value of the type I and III interferon (显示 IFNA 蛋白) subtypes (alphas, beta and lambdas) as therapeutics for prevention and treatment of viral infections (influenza, herpes, human immunodeficiency virus and hepatitis viruses).

9. 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.

10. c-Cbl (显示 CBL 蛋白) negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 (显示 IRF3 蛋白) ubiquitination and degradation.

Mouse (Murine) Interferon, beta 1, Fibroblast (IFNB1) interaction partners

1. Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNbeta, which induced beta-cell apoptosis by increasing the expression of Xaf1 (显示 XAF1 蛋白).

2. Reactive oxygen species (ROS (显示 ROS1 蛋白)) 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 (显示 ROS1 蛋白) in dermatomyositis .

3. Nontypeable Haemophilus influenzae DNA as a Pathogen-Associated Molecular Pattern Molecules triggered I-IFN response, which was STING/TBK1 (显示 TBK1 蛋白)/IRF3 (显示 IRF3 蛋白) dependent.

4. The Lipopolysaccharide and IFN-beta-mediated increase of STAT1 (显示 STAT1 蛋白) 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.

5. MAVS (显示 MAVS 蛋白) is essential for spontaneous high basal expression of IFN-beta in cardiac myocytes and the heart.

6. Mycobacterium smegmatis induces higher Ifnb expression in macrophages than Mycobacterium avium subspecies.

7. In experimental autoimmune encephalomyelitis, IFN-beta inhibited downstream inflammatory cytokines through the inhibition of PI3K/AKT (显示 AKT1 蛋白)/NF-kappaB (显示 NFKB1 蛋白) axis and p38 (显示 CRK 蛋白), JNK (显示 MAPK8 蛋白)-MAPK (显示 MAPK1 蛋白), as well as the regulation of mTOR (显示 FRAP1 蛋白) complexes. Moreover, IFN-beta inhibited Th17 differentiation and influenced the acetylation of the Il17a (显示 IL17A 蛋白) and Opn (显示 SPP1 蛋白) gene promoters. IFN-beta plays a role in Th17 differentiation partly through the inhibition of OPN (显示 SPP1 蛋白).

8. 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.

9. 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.

10. c-Cbl (显示 CBL 蛋白) negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 (显示 IRF3 蛋白) ubiquitination and degradation.

Cow (Bovine) Interferon, beta 1, Fibroblast (IFNB1) interaction partners

1. BVDV2-E significantly increased IFN-beta activity compared to BVDV2-wt.

2. The data confirm the involvement of EHMT2 (显示 EHMT2 蛋白) in the epigenetic regulation of IFN-b and demonstrate the activation of a general antiviral state after EHMT2 (显示 EHMT2 蛋白) inhibition.

3. 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).

4. The authors demonstrate that bovine herpesvirus 1 bICP0 effectively inhibits bovine IFN-beta promoter activity and induces IRF3 (显示 IRF3 蛋白) degradation.

5. These studies provide evidence that virus infection differentially stimulates expression of the three bovine IFN-beta genes.

6. recombinant bovine respiratory syncytial virus lacking the NS proteins, and those lacking NS2 in particular, are strong inducers of IFN-alpha (显示 IFNA 蛋白)/beta in bovine nasal fibroblasts and bronchoalveolar macrophages.

Pig (Porcine) Interferon, beta 1, Fibroblast (IFNB1) interaction partners

1. These results indicate that porcine circovirus type 2 disrupts the interaction of KPNA3 (显示 KPNA3 蛋白) with p-IRF3 (显示 IRF3 蛋白) and blocks p-IRF3 (显示 IRF3 蛋白) translocation to the nucleus, thereby inhibiting IFN-beta induction in PK-15 cells.

2. Nuclear export of NSP1alpha of porcine reproductive and respiratory syndrome virus was necessary for its ability for IFN beta inhibition.

3. Porcine deltacoronavirus nsp5 (显示 SPECC1 蛋白), the 3C-like protease, inhibits interferon-beta production through the cleavage of NEMO (显示 IKBKG 蛋白).

4. Highly pathogenic Porcine reproductive and respiratory syndrome virus modulates Interferon-beta expression mainly through attenuating IRF-3 (显示 IRF3 蛋白) phosphorylation.

5. Porcine epidemic diarrhea virus nsp1 inhibited the IFN-beta and IRF3 (显示 IRF3 蛋白) promoter activities.

6. poIFIT3 plays a significant role in the clearance of swine influenza virus in pigs and potentiates IFN-beta production.

7. DDX41 (显示 DDX41 蛋白) is involved in the dsDNA- and dsDNA-virus-mediated type IFN-beta signaling pathway in porcine kidney cells.

8. VIral NS4 (显示 SOS1 蛋白) protein antagonizes beta interferon (显示 IFNA 蛋白) expression by targeting the NF-kappaB (显示 NFKB1 蛋白) essential modulator.

9. Swine IFN-beta promotes genetic mutation of porcine reproductive and respiratory syndrome virus.

10. Expression of LSm14A (显示 LSM14A 蛋白) in HEK293 or Marc (显示 CCL7 蛋白)-145 cells enhanced activities of IFN-beta and NF-kappaB (显示 NFKB1 蛋白) promoters, induced IFN-beta transcription, and potentiated IFN-beta promoter activation, indicating that LSm14A (显示 LSM14A 蛋白) is a potential signal molecule (显示 WNT4 蛋白) in the IFN-beta pathway.

Rhesus Monkey Interferon, beta 1, Fibroblast (IFNB1) interaction partners

1. 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

2. Hepatitis A virus protein 2B suppresses beta interferon (显示 IFNA 蛋白) (IFN) gene transcription by interfering with IFN regulatory factor 3 activation.