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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Interferon, alpha 6

IFNA6, interferon alpha 54, interferon-alpha 6, interferon alpha K
Top mentioned proteins: IFNA5, V1a, Interferon-alpha, Interferon-beta, HAD
Papers on IFNA6
Expression patterns of immune-associated genes in external genital and perianal warts treated with sinecatechins.
Tyring et al., Houston, United States. In Viral Immunol, May 2015
Genes that were significantly regulated between VRs and VNRs were CREB3L4, HIST1H3A, HIST1H3H, IFNA1, IFNA4, IFNA5, IFNA6, IFNA8, IFNA14, IFNG, IFNAR1, IL6, IRF9, MAPK4, MAPK5, MAPK14, NET1, and PIK3C2A in the IFN array.
Expression of B-cell-associated genes in peripheral blood mononuclear cells of patients with symptomatic pulmonary embolism.
Song et al., Shanghai, China. In Mol Med Report, Mar 2015
Furthermore, the expression levels of B‑cell‑activation‑associated cytokine genes demonstrated a significant upregulation of LTA and IL10 and downregulation of L1A, IFNA5, IFNA6, IFNA8, IFNA14, IL2, IL13 and IFNG in PE patients compared to those of the control group.
Mental quality of life is related to a cytokine genetic pathway.
Zwinderman et al., Amsterdam, Netherlands. In Plos One, 2011
Patients with lower MCS scores had high expression levels of CXCL9 and CXCL11 cytokine-related genes (p=0.001; p=0.002); similarly, patients with low vitality scores had high expression levels of CXCL9, CXCL11 and IFNA6 cytokine-related genes (p=0.02; p=0.02; p=0.04), independent of patient characteristics.
Lymphocytoid choriomeningitis virus activates plasmacytoid dendritic cells and induces a cytotoxic T-cell response via MyD88.
Akira et al., Suita, Japan. In J Virol, 2008
Analysis of Ifna6(+/GFP) reporter mice revealed that plasmacytoid dendritic cells (DCs) are the major source of IFN-alpha in LCMV infection.
Alveolar macrophages are the primary interferon-alpha producer in pulmonary infection with RNA viruses.
Akira et al., Suita, Japan. In Immunity, 2007
Here we generated a knockin mouse in which green fluorescence protein (GFP) was expressed under the control of the Ifna6 promoter.
Differential activities of alpha/beta IFN subtypes against influenza virus in vivo and enhancement of specific immune responses in DNA vaccinated mice expressing haemagglutinin and nucleoprotein.
Bartlett et al., Perth, Australia. In Vaccine, 2007
Differences in antiviral efficacy were found among the subtypes with IFNA5 and IFNA6 being most effective, while IFNA1 was the least effective in reducing lung virus replication.
Type I IFN-beta gene therapy suppresses cardiac CD8+ T-cell infiltration during autoimmune myocarditis.
James et al., Australia. In Immunol Cell Biol, 2004
Gene therapy using DNA encoding type I IFN subtypes IFNA6, IFNA9 and IFNB suppresses murine cytomegalovirus (MCMV)-myocarditis, a predominantly cell-mediated disease in BALB/c mice.
Cytokine expression in murine cytomegalovirus-induced myocarditis: modulation with interferon-alpha therapy.
James et al., Perth, Australia. In Cell Immunol, 2003
During the chronic phase of disease, IFNA6 DNA treatment in vivo increased IL-18 production in the heart.
Type I interferon differential therapy for erythroleukemia: specificity of STAT activation.
James et al., Perth, Australia. In Blood, 2003
IFN subtypes differentially regulated the onset of erythroleukemia with delayed onset and increased survival, possibly via a reduction in cell viability, and enhanced antiproliferative and apoptotic effects observed for IFNA6 and IFNA9 treatment, respectively.
Synergy of type I interferon-A6 and interferon-B naked DNA immunotherapy for cytomegalovirus infection.
James et al., Australia. In Immunol Cell Biol, 2002
Only IFN-A6/A9 and IFN-A9/B reduced acute viral myocarditis, whereas IFNA6/B treatment was most efficacious for autoimmune chronic myocarditis.
Type I interferon gene therapy protects against cytomegalovirus-induced myocarditis.
James et al., Perth, Australia. In Immunology, 2002
IFNA6 treatment reduced MCMV replication whilst IFNA5 and A2 enhanced virus replication.
Randomized clinical trial of long-term outcome after resection of hepatitis C virus-related hepatocellular carcinoma by postoperative interferon therapy.
Kinoshita et al., Ōsaka, Japan. In Br J Surg, 2002
Patients in the interferon group received interferon-alpha 6 MIU intramuscularly every day for 2 weeks, then three times a week for 14 weeks and finally twice a week for 88 weeks.
Cutaneous metastases in renal cell carcinoma.
Gupta et al., New Delhi, India. In Urol Int, 1998
4 patients were treated with interferon-alpha 6 MIU, subcutaneously, three times a week for varying periods from 3 to 4 months but there was no response.
Alpha interferon suppresses the cyclin D3 and cdc25A genes, leading to a reversible G0-like arrest.
Kimchi et al., Israel. In Mol Cell Biol, 1996
Alpha interferon suppresses the cyclin D3 and cdc25A genes, leading to a reversible G0-like arrest.
Stimulation of interferon and cytokine gene expression by imiquimod and stimulation by Sendai virus utilize similar signal transduction pathways.
Pitha et al., Baltimore, United States. In Mol Cell Biol, 1995
In this study, we show that, in these cells, imiquimod induces expression of several IFNA genes (IFNA1, IFNA2, IFNA5, IFNA6, and IFNA8) as well as the IFNB gene.
Virus-mediated induction of interferon A gene requires cooperation between multiple binding factors in the interferon alpha promoter region.
Pitha et al., Baltimore, United States. In J Biol Chem, 1993
Interestingly, our data also show that the inability of IFNA6 promoter to be expressed in infected L-cells may be a result of a viral-induced repressor, which could act by binding and inactivating alpha F1 or by competing for the IRF-1 binding site.
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