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Human IFNA1 Protein expressed in Escherichia coli (E. coli) - ABIN413375
Sen, Che, Rajamani, Zerboni, Sung, Ptacek, Arvin: Signal transducer and activator of transcription 3 (STAT3) and survivin induction by varicella-zoster virus promote replication and skin pathogenesis. in Proceedings of the National Academy of Sciences of the United States of America 2012
Taken together, this work suggests that IFNa (show IFNA Proteins) provides protection of salmon against SAV3 locally in an infected area while IFNb (show IFNB1 Proteins) and IFNc provides systemic protection against the virus.
IFNa (show IFNA Proteins) is the main IFN subtype induced through salmon RIG-I (show DDX58 Proteins)/viral RNA receptor MDA5 (show IFIH1 Proteins) pathway in lymphoid tissues.
These findings also identify STAT3 (show STAT3 Proteins) as a therapeutic target against viral infection and highlight it as an essential pathway component for endogenous and therapeutic IFN-alpha (show IFNA Proteins) responsiveness.
the close association between the increased proportion of CD180 (show CD180 Proteins)-negative B cells and the activation of IFN-alpha (show IFNA Proteins) signaling in Systemic lupus erythematosus, is reported.
IL-12 (show IL12A Proteins) and IFN-alpha (show IFNA Proteins) differentially program CD8 (show CD8A Proteins) T cells to re-express distinct levels of PD-1 (show PDCD1 Proteins) upon re-encountering Ag, resulting in IL-12 (show IL12A Proteins)-stimulated cells being less susceptible to exhaustion in the face of sustained tumor Ag.
The expansion of CD8 (show CD8A Proteins) T cells depends on type I IFN, type I IFN and IL-12 (show IL12A Proteins) or is largely independent of the two cytokines.
A spontaneous genomic duplication and frameshift mutation in the guanine exchange factor dedicator of cytokinesis 2 (Dock2) that has arisen in at least a subset of circulating Irf5(-/-) mice and inadvertently been bred to homozygosity.
Knockdown of endogenous guanylate binding protein (GBP)4 (show GBP4 Proteins) increases IRF7 (show IRF7 Proteins)-mediated IFN-alpha (show IFNA Proteins) production, whereas overexpression of GBP4 (show GBP4 Proteins) has the opposite effect.
Data show that similar T cell expansion and serum IgG responses were observed in adenovirus (Adv (show AVIL Proteins))-IFN-treated WT and BAFF (show TNFSF13B Proteins)-deficient mice despite their disparate pathological and clinical responses.
Studies in both mice and humans have demonstrated a role for IFN-alpha (show IFNA Proteins)/beta in directly influencing the fate of both CD4 (show CD4 Proteins)(+) and CD8 (show CD8A Proteins)(+) T cells during the initial phases of antigen recognition.
IFN-alpha (show IFNA Proteins) enhances both the induction and maintenance of programmed cell death (PD)-1 (show PDCD1 Proteins) expression on T cell receptor-engaged primary mouse T cells through association of IFN-responsive factor 9 (IRF9 (show IRF9 Proteins)) with the IFN stimulation response element.
This article reports the production of interferon alpha (show IFNA Proteins)/beta (IFN-alpha (show IFNA Proteins)/beta) by SJL/J mouse brain astrocyte cultures infected with Theiler's murine encephalomyelitis virus (TMEV).
Study shows IFN-alpha (show IFNA Proteins) rapidly induces a profound shift in whole brain network structure, impairing global functional connectivity and the efficiency of parallel information exchange.
The review focuses on the value of the type I and III interferon (show IFNA Proteins) subtypes (alphas, beta and lambdas) as therapeutics for prevention and treatment of viral infections (influenza, herpes, human immunodeficiency virus and hepatitis viruses).
MiR (show MLXIP Proteins)-181a is an important mediator for interferons-induced SAMHD1 (show SAMHD1 Proteins) expression in astrocytes and microglia, but not for inhibition of HIV-1 infection induced by IFN-alpha (show IFNA Proteins).
the expression of certain TAM (show CCNA1 Proteins) components was reduced as a result of prolonged degradation of MYD88 (show MYD88 Proteins) by Porphyromonas gingivalis infection.
Type I interferons (IFNs) signature is seen in a significant proportion of anti-nuclear antibody-positive (ANA (show BTG3 Proteins)(+) individuals and appears to be associated with ANA (show BTG3 Proteins) titre and type of autoantibodies, rather than with the presence or development of clinical systemic autoimmune rheumatic diseases (SARDs) symptoms.
study found that endogenous IFNalpha autocrinally promotes the expression of Interferon (show IFNA Proteins)-Stimulated Gene (ISG) mRNAs in IL-3 (show IL-3 Proteins)-, but not in IFNlambda3 plus IL-3 (show IL-3 Proteins)-, treated plasmacytoid dendritic cells (pDCs); production of IFNalpha by IFNlambda3 plus IL-3 (show IL-3 Proteins)-treated pDCs is mostly dependent on endogenously produced TNFalpha (show TNF Proteins)
results demonstrate that Sphingosine 1-phosphate lyase (SPL (show SGPL1 Proteins)) is a host factor that augments type I IFN responses during influenza A virus infection; study delineates the relationship between IKKepsilon (show IKBKE Proteins) and SPL (show SGPL1 Proteins), which provides a mechanistic understanding of the pro-IFN activity of SPL (show SGPL1 Proteins)
These data suggest that plasmacytoid dendritic cells producing IFN-alpha (show IFNA Proteins) and IL-33 (show IL33 Proteins) play a pivotal role in the chronic fibro-inflammatory responses underlying murine autoimmune pancreatitis and human IgG4-related autoimmune pancreatitis.
Mothers of children affected by autoimmune congenital heart block had a significantly higher expression IFN-alpha (show IFNA Proteins).
Collectively, these data show that porcine epidemic diarrhea virus is capable of subverting the type I interferon (show IFNA Proteins) response by inducing STAT1 (show STAT1 Proteins) degradation.
Amino acid residues in the N-terminal domain of Npro are involved in the stability of Npro, in interaction of Npro with IRF-3 (show IRF3 Proteins) and subsequent degradation of IRF-3 (show IRF3 Proteins), leading to downregulation of IFN-alpha (show IFNA Proteins)/beta production.
Pregnane X receptor is required for interferon-alpha-mediated CYP3A29 expression, and its expression before CYP3A29.
Overall, data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-alpha (show IFNA Proteins)/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha (show IFNA Proteins) in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.
Nsp1beta inhibits interferon-activated (show MNDA Proteins) STAT1 (show STAT1 Proteins)/STAT2 (show STAT2 Proteins) signal transduction by inducing karyopherin-alpha1 degradation.
Expression of Mx protein (show MX2 Proteins) and interferon-alpha (IFN-alpha (show IFNA Proteins)) was examined by immunohistochemistry in pigs experimentally infected with swine influenza virus.
Foot-and-Mouth Disease Virus inhibits IFN-alpha (show IFNA Proteins) expression in infected cells by blocking cap-dependent translation.
The protein encoded by this gene is produced by macrophages and has antiviral activity. This gene is intronless and the encoded protein is secreted.
, interferon alpha 1
, interferon alpha 13
, interferon alpha family gene 1
, interferon alpha-1
, IFN-alpha 1
, interferon-alpha 1
, IFN-alpha 1b
, interferon alpha 1b
, interferon alpha-D
, leIF D