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Human IFNA Protein expressed in Escherichia coli (E. coli) - ABIN803851
Goetzl, Huang, Kon, Patel, Schwartz, Fast, Ferrucci, Madara, Taub, Longo: Gender specificity of altered human immune cytokine profiles in aging. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2010
the polymorphic variant of IFNA1 (show IFNA1 Proteins) (-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 (show XBP1 Proteins) in TLR7 (show TLR7 Proteins)-induced IFNalpha production and identify XBP1 (show XBP1 Proteins) 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 (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.
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-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)
The TBK1 (show TBK1 Proteins) Y179A mutant failed to rescue type I IFN production by virally infected RAW264.7 macrophages deficient in TBK1 (show TBK1 Proteins).
this study introduces a novel pathway by which IFN-alpha serves as a proatherogenic mediator through repression of eNOS (show NOS3 Proteins)-dependent pathways
study reports that mitochondrial antiviral signaling protein (MAVS (show MAVS Proteins)), -mediated IFN-alpha/beta production and IFNAR (show IFNAR1 Proteins) signaling are required for alloimmune responses to the human K1 Ag in a murine model of inflammation-induced alloimmunization
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 responsiveness.
CD169 (show SIGLEC1 Proteins)(+) macrophages are important contributors to the IFN-I response and thereby influence antiviral activity, CD8 (show CD8A Proteins)(+) T-cell exhaustion and immunopathology.
These results suggest that pulmonary C-fibers affect IFNGR1 (show IFNGR1 Proteins) expression by inducing IFN-alpha to regulate IFN-gamma (show IFNG Proteins)-mediated airway inflammation and airway hyperresponsiveness.
results show that resistance to HSV-1 in the trigeminal ganglia during acute infection is conferred in part by STING and IFN-alpha/beta signaling in both bone marrow-derived and -resident cells, which coalesce to support a robust HSV-1-specific CD8 (show CD8A Proteins)(+) T cell response
the close association between the increased proportion of CD180 (show CD180 Proteins)-negative B cells and the activation of IFN-alpha signaling in Systemic lupus erythematosus, is reported.
STAT2 (show STAT2 Proteins) recruits USP18 (show USP18 Proteins) to the type I IFN receptor subunit IFNAR2 (show IFNAR2 Proteins) via its constitutive membrane-distal STAT2 (show STAT2 Proteins)-binding site.
Collectively, these data show that porcine epidemic diarrhea virus is capable of subverting the type I interferon 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/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/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 (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) 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.
produced in vitro and in vivo in response to noncytopathic bovine viral diarrhea virus in lymph nodes cells expressing the myeloid markers CD14 (show CD14 Proteins), CD11b (show ITGAM Proteins), and CD172a (show SIRPA Proteins)
Prolonged treatment with IFN-alpha (12-48 h) resulted in increased expression of STAT1 (show STAT1 Proteins) and, to a lesser extent, STAT2 (show STAT2 Proteins).
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
, interferon alpha 7
, IFN-alpha 1b
, interferon alpha 1b
, interferon alpha-1/13
, interferon alpha-D
, leIF D
, interferon alpha family gene 1
, interferon alpha-1
, interferon alpha 1
, IFN alpha
, interferon type A1/A2
, interferon type A3
, interferon alpha A
, Interferon alpha-1