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anti-Human IFNA1 Anticorps:
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the state of type I IFN induction and response to, in SAMHD1 knockout (KO) human monocytic cells, was examined.
hypoxia triggers the production of IFN-I in vitro, and may contribute to the pathogenesis of dermatomyositis together with other inflammatory factors.
SOCS2 impairs IFN/JAK/STAT signaling through reducing the stability of tyrosine kinase 2 (TYK2), downregulating the expression of type I and III IFN receptors, attenuating the phosphorylation and nucleus translocation of STAT1.
Significant associations were observed for 4 variants in IFNAR2, IFNLR1 with hepatitis B virus infection, and IFNLR1-rs4649203 was associated with hepatitis B recovery. Moreover, the authors demonstrated the clear relevance of 5 polymorphisms in IFNA1, IFNA2, IFNL4 with hepatocellular carcinoma.
HIV-1 IIIB infection of myeloid ThP-1 cells also reduced the IFN-alpha-mediated induction of the anti-viral gene, ISG15, but not MxA, revealing a functional consequence of this HIV-1-mediated immune evasion strategy.
Therefore, these results demonstrate the importance of MxB in alpha interferon-mediated inhibition of HIV-1 infection.
Our results illustrate a novel regulatory role of TWEAK, in which its activity positively regulates type I IFN pathway in lupus nephritis (LN) based on preclinical models. Our findings suggest TWEAK could act as a critical target in preventing renal damage in patients with LN.
Myeloid cells contribute more to the whole blood interferon signature in systemic lupus erythematosus than their lymphocytic counterpart. Very similar leukocyte subsets reveal distinctive IFN signatures. IFN alpha mixes up composition of blood and leads to a preferential neutropenia, yielding relative lymphocytosis.
the polymorphic variant of IFNA1 (-2) gene is associated with chronic HBV infection
Cerebrospinal fluid interferon alpha levels correlate with neurocognitive impairment in ambulatory HIV-Infected individuals.
Data suggest a central role of XBP1 in TLR7-induced IFNalpha production and identify XBP1 as a potential novel therapeutic target in IFNalpha-driven autoimmune and inflammatory diseases.
Study shows IFN-alpha 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 subtypes (alphas, beta and lambdas) as therapeutics for prevention and treatment of viral infections (influenza, herpes, human immunodeficiency virus and hepatitis viruses).
MiR-181a is an important mediator for interferons-induced SAMHD1 expression in astrocytes and microglia, but not for inhibition of HIV-1 infection induced by IFN-alpha.
the expression of certain TAM components was reduced as a result of prolonged degradation of MYD88 by Porphyromonas gingivalis infection.
Type I interferons (IFNs) signature is seen in a significant proportion of anti-nuclear antibody-positive (ANA(+) individuals and appears to be associated with ANA 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-Stimulated Gene (ISG) mRNAs in IL-3-, but not in IFNlambda3 plus IL-3-, treated plasmacytoid dendritic cells (pDCs); production of IFNalpha by IFNlambda3 plus IL-3-treated pDCs is mostly dependent on endogenously produced TNFalpha
results demonstrate that Sphingosine 1-phosphate lyase (SPL) is a host factor that augments type I IFN responses during influenza A virus infection; study delineates the relationship between IKKepsilon and SPL, which provides a mechanistic understanding of the pro-IFN activity of SPL
These data suggest that plasmacytoid dendritic cells producing IFN-alpha and IL-33 play a pivotal role in the chronic fibro-inflammatory responses underlying murine autoimmune pancreatitis and human IgG4-related autoimmune pancreatitis.
These findings also identify STAT3 as a therapeutic target against viral infection and highlight it as an essential pathway component for endogenous and therapeutic IFN-alpha responsiveness.
the close association between the increased proportion of CD180-negative B cells and the activation of IFN-alpha signaling in Systemic lupus erythematosus, is reported.
IL-12 and IFN-alpha differentially program CD8 T cells to re-express distinct levels of PD-1 upon re-encountering Ag, resulting in IL-12-stimulated cells being less susceptible to exhaustion in the face of sustained tumor Ag.
The expansion of CD8 T cells depends on type I IFN, type I IFN and IL-12 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 increases IRF7-mediated IFN-alpha production, whereas overexpression of GBP4 has the opposite effect.
protects against antigen-induced arthritis
Data show that similar T cell expansion and serum IgG responses were observed in adenovirus (Adv)-IFN-treated WT and BAFF-deficient mice despite their disparate pathological and clinical responses.
Studies in both mice and humans have demonstrated a role for IFN-alpha/beta in directly influencing the fate of both CD4(+) and CD8(+) T cells during the initial phases of antigen recognition.
IFN-alpha enhances both the induction and maintenance of programmed cell death (PD)-1 expression on T cell receptor-engaged primary mouse T cells through association of IFN-responsive factor 9 (IRF9) with the IFN stimulation response element.
This article reports the production of interferon alpha/beta (IFN-alpha/beta) by SJL/J mouse brain astrocyte cultures infected with Theiler's murine encephalomyelitis virus (TMEV).
TLR ligands facilitate antibody response by inducing type I interferon (IFN), which in turn elicits rapid and significant amounts of antigen-specific IgG2c.
These results demonstrate that mouse hepatitis virus is recognized by both RIG-I and MDA5 and induces IFN-alpha/beta through the activation of the IRF-3 signaling pathway.
Sufficient IFN-alpha production by plasmacytoid dentritic cells is an important determinant of vaccine efficacy.
B cell-mediated type I IFN induction depended on the transcription factor IRF3.
The involvement of IRF1 and IRF2 in TLR2-mediated responses, was studied.
Report that tumor-targeted interferon-alpha1 delivery by Tie2-expressing monocytes inhibits tumor growth and metastasis.
It is likely that IFN-alpha plays a complex role in the etiology of type 1 diabetes.
Collectively, these findings demonstrate that constitutive and LPS-induced type I IFN play significant roles in regulating the differences in phenotype and function between BMM and GM-BMM.
Recombinant IFN-alpha treatment promotes monocyte chemoattractant protein (MCP)-1, MCP-5, and, to a lesser extent, MCP-3 production in the bone marrow during murocytomegalovirus infection.
Thus, we assume that IFNalpha, produced after porcine reproductive and respiratory syndrome virus infection, could affect the immune response of monocyte-derived macrophages.
Collectively, these data show that porcine epidemic diarrhea virus is capable of subverting the type I interferon response by inducing STAT1 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 and subsequent degradation of IRF-3, leading to downregulation of IFN-alpha/beta production.
Pregnane X receptor is required for interferon-alpha-mediated CYP3A29 expression, and its expression before CYP3A29.
These data suggest that porcine reproductive and respiratory syndrome virus nsp1beta may selectively suppress cellular gene expression, including expression of genes involved in the host innate immune function.
Overall, data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-alpha/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.
Nsp1beta inhibits interferon-activated STAT1/STAT2 signal transduction by inducing karyopherin-alpha1 degradation.
Expression of Mx protein and interferon-alpha (IFN-alpha) was examined by immunohistochemistry in pigs experimentally infected with swine influenza virus.
Foot-and-Mouth Disease Virus inhibits IFN-alpha expression in infected cells by blocking cap-dependent translation.
Taken together, this work suggests that IFNa provides protection of salmon against SAV3 locally in an infected area while IFNb and IFNc provides systemic protection against the virus.
IFNa is the main IFN subtype induced through salmon RIG-I/viral RNA receptor MDA5 pathway in lymphoid tissues.
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 1b
, interferon alpha-1/13
, interferon alpha-D
, leIF D
, interferon alpha family gene 1
, interferon alpha-1
, interferon alpha 1
, interferon alpha 13
, IFN alpha
, interferon alpha
, interferon type A1/A2
, interferon type A3