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anti-Mouse (Murine) IFNA1 Antibodies:
anti-Rat (Rattus) IFNA1 Antibodies:
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Taken together, this work suggests that IFNa (show IFNA Antibodies) provides protection of salmon against SAV3 locally in an infected area while IFNb (show IFNB1 Antibodies) and IFNc provides systemic protection against the virus.
IFNa (show IFNA Antibodies) is the main IFN subtype induced through salmon RIG-I (show DDX58 Antibodies)/viral RNA receptor MDA5 (show IFIH1 Antibodies) pathway in lymphoid tissues.
These findings also identify STAT3 (show STAT3 Antibodies) as a therapeutic target against viral infection and highlight it as an essential pathway component for endogenous and therapeutic IFN-alpha (show IFNA Antibodies) responsiveness.
the close association between the increased proportion of CD180 (show CD180 Antibodies)-negative B cells and the activation of IFN-alpha (show IFNA Antibodies) signaling in Systemic lupus erythematosus, is reported.
IL-12 (show IL12A Antibodies) and IFN-alpha (show IFNA Antibodies) differentially program CD8 (show CD8A Antibodies) T cells to re-express distinct levels of PD-1 (show PDCD1 Antibodies) upon re-encountering Ag, resulting in IL-12 (show IL12A Antibodies)-stimulated cells being less susceptible to exhaustion in the face of sustained tumor Ag.
The expansion of CD8 (show CD8A Antibodies) T cells depends on type I IFN, type I IFN and IL-12 (show IL12A Antibodies) 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 (show DOCK2 Antibodies)) that has arisen in at least a subset of circulating Irf5 (show IRF5 Antibodies)(-/-) mice and inadvertently been bred to homozygosity.
Knockdown of endogenous guanylate binding protein (GBP)4 (show GBP4 Antibodies) increases IRF7 (show IRF7 Antibodies)-mediated IFN-alpha (show IFNA Antibodies) production, whereas overexpression of GBP4 (show GBP4 Antibodies) has the opposite effect.
Data show that similar T cell expansion and serum IgG responses were observed in adenovirus (Adv (show AVIL Antibodies))-IFN-treated WT and BAFF (show TNFSF13B Antibodies)-deficient mice despite their disparate pathological and clinical responses.
Studies in both mice and humans have demonstrated a role for IFN-alpha (show IFNA Antibodies)/beta in directly influencing the fate of both CD4 (show CD4 Antibodies)(+) and CD8 (show CD8A Antibodies)(+) T cells during the initial phases of antigen recognition.
IFN-alpha (show IFNA Antibodies) enhances both the induction and maintenance of programmed cell death (PD)-1 (show PDCD1 Antibodies) expression on T cell receptor-engaged primary mouse T cells through association of IFN-responsive factor 9 (IRF9 (show IRF9 Antibodies)) with the IFN stimulation response element.
This article reports the production of interferon alpha (show IFNA Antibodies)/beta (IFN-alpha (show IFNA Antibodies)/beta) by SJL/J mouse brain astrocyte cultures infected with Theiler's murine encephalomyelitis virus (TMEV).
the expression of certain TAM (show CCNA1 Antibodies) components was reduced as a result of prolonged degradation of MYD88 (show MYD88 Antibodies) by Porphyromonas gingivalis infection.
Type I interferons (IFNs) signature is seen in a significant proportion of anti-nuclear antibody-positive (ANA (show BTG3 Antibodies)(+) individuals and appears to be associated with ANA (show BTG3 Antibodies) 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 Antibodies)-Stimulated Gene (ISG) mRNAs in IL-3 (show IL-3 Antibodies)-, but not in IFNlambda3 plus IL-3 (show IL-3 Antibodies)-, treated plasmacytoid dendritic cells (pDCs); production of IFNalpha by IFNlambda3 plus IL-3 (show IL-3 Antibodies)-treated pDCs is mostly dependent on endogenously produced TNFalpha (show TNF Antibodies)
results demonstrate that Sphingosine 1-phosphate lyase (SPL (show SGPL1 Antibodies)) is a host factor that augments type I IFN responses during influenza A virus infection; study delineates the relationship between IKKepsilon (show IKBKE Antibodies) and SPL (show SGPL1 Antibodies), which provides a mechanistic understanding of the pro-IFN activity of SPL (show SGPL1 Antibodies)
These data suggest that plasmacytoid dendritic cells producing IFN-alpha (show IFNA Antibodies) and IL-33 (show IL33 Antibodies) 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 Antibodies).
Suppression of the exogenous Type I IFN-induced Jak (show JAK3 Antibodies)/STAT (show STAT1 Antibodies) signaling by NSs might be one of the mechanisms of Severe fever with thrombocytopenia syndrome (SFTS) to evade host immune surveillance.
High Type I Interferon (show IFNA Antibodies) expression due to hypomethylation is associated with Systemic Lupus Erythematosus.
these studies identify phosphorylation of S734-STAT2 (show STAT2 Antibodies) as a new regulatory mechanism that negatively controls the type I IFN-antiviral response.
Collectively, these data show that porcine epidemic diarrhea virus is capable of subverting the type I interferon (show IFNA Antibodies) response by inducing STAT1 (show STAT1 Antibodies) 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 Antibodies) and subsequent degradation of IRF-3 (show IRF3 Antibodies), leading to downregulation of IFN-alpha (show IFNA Antibodies)/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 Antibodies)/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha (show IFNA Antibodies) in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.
Nsp1beta inhibits interferon-activated (show MNDA Antibodies) STAT1 (show STAT1 Antibodies)/STAT2 (show STAT2 Antibodies) signal transduction by inducing karyopherin-alpha1 degradation.
Expression of Mx protein (show MX2 Antibodies) and interferon-alpha (IFN-alpha (show IFNA Antibodies)) was examined by immunohistochemistry in pigs experimentally infected with swine influenza virus.
Foot-and-Mouth Disease Virus inhibits IFN-alpha (show IFNA Antibodies) 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