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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 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)
These data suggest that plasmacytoid dendritic cells producing IFN-alpha 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.
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.
Mothers of children affected by autoimmune congenital heart block had a significantly higher expression IFN-alpha.
Suppression of the exogenous Type I IFN-induced Jak (show JAK3 Proteins)/STAT (show STAT1 Proteins) 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 expression due to hypomethylation is associated with Systemic Lupus Erythematosus.
these studies identify phosphorylation of S734-STAT2 (show STAT2 Proteins) 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 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.
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
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
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.
In the exorbital lachrymal gland, the mRNA expression of IFN beta and IFN alpha (type I IFNs) was weak- to strong-positive at 1 days post inoculation (DPI), and became negative at 2DPI.
IRF-1 (show IRF1 Proteins) and interferon-alpha with interferon-beta (show IFNB1 Proteins) cooperate to control acute gammaherpesvirus infection.
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 1b
, interferon alpha-1/13
, interferon alpha-D
, leIF D
, interferon alpha 1
, interferon alpha-1
, interferon alpha A