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18 documents found
1: Title: Integrated analysis of microRNA-mRNA expression in A549 cells infected with influenza A viruses (IAVs) from different host species.
Authors: Gao, Jie, et.al. .
Journal: Virus research (Virus Res), Vol. 263, 2018 .
Snippet: Additionally, the obtained results were supported by an RT-qPCR analysis of 8 differentially expressed miRNAs (hsa-miR-210-3p, hsa-miR-296-5p, hsa-miR-371a-5p, hsa-miR-762, hsa-miR-937-5p, hsa-miR-1915-3p, hsa-miR-3665, and hsa-miR-1290) and 13 differentially expressed mRNAs (IFNL1, CXCL10, RSAD2, MX1, OAS2, IFIT2, IFI44 L, MX2, XAF1, NDRG1, FGA, EGLN3, and TFRC).
Affiliation: Department of Microbiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, 530021, China. Department of Microbiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, 530021, China. Electronic address: fanxiaohui63@163.com. .
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2: Title: IL28B, IL29 and micro-RNA 548 in subacute sclerosing panencephalitis as a rare disease.
Authors: Cakmak Genc, Gunes, et.al. .
Journal: Gene, Vol. 678, 2018 .
Snippet: IL-29 expression is thought to be regulated at post-transcriptional level and miRNA-548 family targets the 3'UTR of the IFNL1 gene.
Affiliation: Faculty of Medicine, Department of Medical Genetics, Bulent Ecevit University, Zonguldak, Turkey. Electronic address: gunes.cak@hotmail.com. Faculty of Medicine, Department of Medical Genetics, Bulent Ecevit University, Zonguldak, Turkey. Faculty of Sciences and Arts, Department of Molecular Biology and Genetics, Bulent Ecevit University, Zonguldak, Turkey. Faculty of Medicine, Department of Pediatric Neurology, Harran University, Sanlıurfa, Turkey. Faculty of Medicine, Department of Biostatistics, Bulent Ecevit University, Zonguldak, Turkey. Faculty of Medicine, Department of Pediatrics, Bulent Ecevit University, Zonguldak, Turkey. .
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3: Title: Hypothiocyanous Acid Suppresses PolyI:C-Induced Antiviral Responses by Modulating IRF3 Phosphorylation in Human Airway Epithelial Cells.
Authors: Nguyen, Thuy Thu, et.al. .
Journal: The Tohoku journal of experimental medicine (Tohoku J Exp Med), Vol. 245 (2): 131-140, 2018 .
Snippet: HOSCN decreased polyI:C-induced apoptosis and the expression levels of IFNB1, IFNL1, IFNL2 and IFNL3 mRNAs.
Affiliation: Department of Health Protection, Graduate School of Medicine, Teikyo University. Asia International Institute of Infectious Disease Control, Teikyo University. .
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4: Title: STING-Dependent Interferon-λ1 Induction in HT29 Cells, a Human Colorectal Cancer Cell Line, After Gamma-Radiation.
Authors: Chen, Jianzhou, et.al. .
Journal: International journal of radiation oncology, biology, physics (Int J Radiat Oncol Biol Phys), Vol. 101 (1): 97-106, 2018 .
Snippet: The induction of IFNL1 was primarily mediated by the cytosolic DNA sensors-STING-TBK1-IRF1 signaling axis, with a lesser contribution from the nuclear factor kappa b signaling in HT29 cells.
Affiliation: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom; Department of Oncology, University of Oxford, Oxford, United Kingdom; Department of Radiation Oncology, Cancer Hospital of Shantou University Medical College, Shantou, China. CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom; Department of Oncology, University of Oxford, Oxford, United Kingdom. CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom; Department of Oncology, University of Oxford, Oxford, United Kingdom; Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands. CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom; Department of Oncology, University of Oxford, Oxford, United Kingdom. Electronic address: ruth.muschel@oncology.ox.ac.uk. .
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5: Title: Serum IFN-λ3 Levels Correlate with Serum Hepatitis C Virus RNA Levels in Symptomatic Patients with Acute Hepatitis C.
Authors: Imoto, Susumu, et.al. .
Journal: Digestive diseases (Basel, Switzerland) (Dig Dis), Vol. 35 (6): 531-540, 2017 .
Snippet: Serum IFNL1, IFN-α, IFN-β, and IFN-γ induced protein-10 (IP-10) levels were assayed using commercial enzyme-linked immunosorbent assay (ELISA) kits.
Affiliation: Department of Gastroenterology, Kobe Asahi Hospital, Kobe, Japan. .
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6: Title: Generation and characterization of interferon-lambda 1-resistant H1N1 influenza A viruses.
Authors: Ilyushina, Natalia A, et.al. .
Journal: PloS one, Vol. 12 (7): e0181999, 2017 .
Snippet: Mutants carrying either K331N alone or S79L and K331N together induced weaker phosphorylation of IFN regulatory factor 3 (IRF3), and, as a consequence, much lower expression of the IFN genes (IFNB1, IFNL1 and IFNL2/3) and proteins (IFN-λ1 and IFN-λ2/3).
Affiliation: Division of Biotechnology Research and Review II, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, United States of America. Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America. Carbohydrate Chemistry Laboratory, Shemyakin Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia. .
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7: Title: The landscape of genetic diseases in Saudi Arabia based on the first 1000 diagnostic panels and exomes.
Authors: Monies, Dorota, et.al. .
Journal: Human genetics (Hum Genet), Vol. 136 (8): 921-939, 2017 .
Snippet: Finally, we have encountered candidate variants in 75 genes (ABHD6, ACY3, ADGRB2, ADGRG7, AGTPBP1, AHNAK2, AKAP6, ASB3, ATXN1L, C17orf62, CABP1, CCDC186, CCP110, CLSTN2, CNTN3, CNTN5, CTNNA2, CWC22, DMAP1, DMKN, DMXL1, DSCAM, DVL2, ECI1, EP400, EPB41L5, FBXL22, GAP43, GEMIN7, GIT1, GRIK4, GRSF1, GTRP1, HID1, IFNL1, KCNC4, LRRC52, MAP7D3, MCTP2, MED26, MPP7, MRPS35, MTDH, MTMR9, NECAP2, NPAT, NRAP, PAX7, PCNX, PLCH2, PLEKHF1, PTPN12, QKI, RILPL2, RIMKLA, RIMS2, RNF213, ROBO1, SEC16A, SIAH1, SIRT2, SLAIN2, SLC22A20, SMDT1, SRRT, SSTR1, ST20, SYT9, TSPAN6, UBR4, VAMP4, VPS36, WDR59, WDYHV1, and WHSC1) not previously linked to human phenotypes and these are presented to accelerate post-publication matchmaking.
Affiliation: Deparment of Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Saudi Human Genome Program, King Abdulaziz City for Science and Technology, Riyadh, Saudi Arabia. Department of Medical Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. Children's Hospital, King Saud Medical City, Riyadh, Saudi Arabia. Department of Neurosciences, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia. Department of Neurosciences, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Department of Pediatric Subspecialties, Children's Hospital, King Fahad Medical City, Riyadh, Saudi Arabia. Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia. Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Department of Obstetrics and Gynecology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Pediatric Department, Al-Jahra Hospital, Ministry of Health, Kuwait, Kuwait. Department of Pediatrics, Children's Hospital, Ain Shams University, Cairo, Egypt. Department of Pediatrics, Dr. Suliman Al Habib Medical Group, Riyadh, Saudi Arabia. Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, Saudi Arabia. Department of Liver Transplantation, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Genetics Department, Sultan Qaboos University Hospital, Muscat, Oman. Department of Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Pediatric Neurology Department, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia. Department of Pediatrics, College of Medicine, King Saud University, Riyadh, Saudi Arabia. Global Eye Care, Specialized Medical Center Hospital, Riyadh, Saudi Arabia. Pediatric Department, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Pediatrics, Security Forces Hospital, Riyadh, Saudi Arabia. Department of Oncology, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia. Medical Genetic Division, Department of Pediatrics, King Abdullah International Medical Research Centre, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Riyadh, Saudi Arabia. Maternity and Children's Hospital, Mecca, Saudi Arabia. Saudi German Hospital, Aseer, Saudi Arabia. Clinical Genetic Division of Human Genetics & Genome Research, National Research Center, Dokki, Giza, Egypt. Taif Children's Hospital, Taif, Saudi Arabia. Neonatology, Al Hammadi Hospital, Riyadh, Saudi Arabia. Department of Obstetrics and Gynaecology, College of Medicine, King Saud University, Riyadh, Saudi Arabia. Medical Diagnostic Laboratory, Riyadh, Saudi Arabia. Department of Pediatrics, King Fahd Hospital of the University, College of Medicine, University of Dammam, Dammam, Saudi Arabia. Deparment of Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. falkuraya@kfshrc.edu.sa]. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. falkuraya@kfshrc.edu.sa]. Saudi Human Genome Program, King Abdulaziz City for Science and Technology, Riyadh, Saudi Arabia. falkuraya@kfshrc.edu.sa]. .
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8: Title: Tumor Necrosis Factor Inhibits Spread of Hepatitis C Virus Among Liver Cells, Independent From Interferons.
Authors: Laidlaw, Stephen M, et.al. .
Journal: Gastroenterology, Vol. 153 (2): 566-578.e5, 2017 .
Snippet: Inhibition was independent of IFNα, IFNβ, IFNL1, IFNL2, or Janus kinase signaling via signal transducer and activator of transcription.
Affiliation: Kennedy Institute of Rheumatology, The University of Oxford, Oxford, United Kingdom; Peter Medawar Building for Pathogen Research, The University of Oxford, Oxford, United Kingdom. Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York. Kennedy Institute of Rheumatology, The University of Oxford, Oxford, United Kingdom. Kennedy Institute of Rheumatology, The University of Oxford, Oxford, United Kingdom; Peter Medawar Building for Pathogen Research, The University of Oxford, Oxford, United Kingdom; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York. Electronic address: lynn.dustin@kennedy.ox.ac.uk. .
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9: Title: Interferon Lambda: Modulating Immunity in Infectious Diseases.
Journal: Frontiers in immunology (Front Immunol), Vol. 8, 2017 .
Snippet: Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes.
Affiliation: Applied Microbiology Research, Department of Biomedicine, University of Basel , Basel , Switzerland. Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Clinical Microbiology, University Hospital Basel, Basel, Switzerland. .
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10: Title: Microbial pathogenesis and type III interferons.
Authors: Cohen, Taylor S, et.al. .
Journal: Cytokine & growth factor reviews (Cytokine Growth Factor Rev), Vol. 29, 2016 .
Snippet: Type I IFNs are appreciated to be important in several viral and bacterial diseases, while the recently identified type III IFNs (IFNL1, IFNL2, IFNL3, IFNL4) have been studied primarily in the context of viral infection.
Affiliation: Department of Infectious Disease, Medimmune, Gaithersburg, MD, USA. Department of Pediatrics, Columbia University, New York, NY, USA. Electronic address: dp2375@cumc.columbia.edu. .
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11: Title: Human H7N9 virus induces a more pronounced pro-inflammatory cytokine but an attenuated interferon response in human bronchial epithelial cells when compared with an epidemiologically-linked chicken H7N9 virus.
Authors: To, Kelvin K W, et.al. .
Journal: Virology journal (Virol J), Vol. 13, 2016 .
Snippet: The infected cell lysate was collected at different time points post-infection for the determination of the levels of pro-inflammatory cytokines (tumor necrosis factor α [TNF-α] and interleukin 6 [IL-6]), anti-inflammatory cytokines (interleukin 10 [IL-10] and transforming growth factor beta [TGF-β]), chemokines (interleukin 8 [IL-8] and monocyte chemoattractant protein 1 [MCP-1]), and interferons (interferon β [IFN-β] and interferon lambda 1 [IFNL1]).
Affiliation: Department of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China. State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong, Hong Kong Special Administrative Region, China. Carol Yu Centre for Infection, The University of Hong Kong, Hong Kong Special Administrative Region, China. Research Centre of Infection and Immunology, The University of Hong Kong, Hong Kong Special Administrative Region, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China. Department of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China. kyyuen@hku.hk. State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong, Hong Kong Special Administrative Region, China. kyyuen@hku.hk. Carol Yu Centre for Infection, The University of Hong Kong, Hong Kong Special Administrative Region, China. kyyuen@hku.hk. Research Centre of Infection and Immunology, The University of Hong Kong, Hong Kong Special Administrative Region, China. kyyuen@hku.hk. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China. kyyuen@hku.hk. .
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12: Title: Achieving sustained virologic response after interferon-free hepatitis C virus treatment correlates with hepatic interferon gene expression changes independent of cirrhosis.
Authors: Meissner, E G, et.al. .
Journal: Journal of viral hepatitis (J Viral Hepat), Vol. 23 (7): 496-505, 2016 .
Snippet: Hepatic gene expression of type III IFNs (IFNL1, IFNL3, IFNL4-ΔG) similarly decreased with treatment, while IFNA2 expression, undetectable in all subjects pretreatment, was detected post-treatment in three subjects who achieved a SVR.
Affiliation: Division of Infectious Diseases, Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Critical Care Medicine Department, NIH Clinical Center, Bethesda, MD, USA. St Joseph's Hospital and Medical Center, Department of Hepatology, Creighton University School of Medicine, Phoenix, AZ, USA. Genomics Unit, Research Technologies Section, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT, USA. Gilead Sciences Inc, Foster City, CA, USA. Division of Clinical Care and Research, Institute of Human Virology, University of Maryland, Baltimore, MD, USA. .
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13: Title: IFNL3 genotype is associated with differential induction of IFNL3 in primary human hepatocytes.
Authors: Kurbanov, Fuat, et.al. .
Journal: Antiviral therapy (Antivir Ther), Vol. 20 (8): 805-14, 2015 .
Snippet: PHH stimulation with cytoplasmic poly I:C induced >1,000-fold expression of IFNL1, IFNL2 and IFNL3.
Affiliation: Division of Infectious Diseases, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA. .
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14: Title: Hepatic expression levels of interferons and interferon-stimulated genes in patients with chronic hepatitis C: A phenotype-genotype correlation study.
Authors: Noureddin, M, et.al. .
Journal: Genes and immunity (Genes Immun), Vol. 16 (5): 321-9, 2015 Jul-Aug .
Snippet: Type I IFNs (IFNA1, IFNB1), type II (IFNG), type III (IFNL1, IFNL2/3), IFNL4 and ISG hepatic expressions were measured by qPCR from in 65 chronic hepatitis C (CHC) patients whose IFNL4-associated rs368234815 and IFNL3-associated rs12989760 genotype were determined.
Affiliation: 1] Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Division of Gastroenterology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. 1] Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Immunology Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. .
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15: Title: IFNL cytokines do not modulate human or murine NK cell functions.
Authors: Morrison, Maria H, et.al. .
Journal: Human immunology (Hum Immunol), Vol. 75 (9): 996-1000, 2014 .
Snippet: Using a range of functional responses, we did not find any evidence of NK cell activation by IFNL3, IFNL1 or IFNL2 cytokines.
Affiliation: Natural Killer Cell Research Group, School of Biochemistry and Immunology, Trinity College Dublin, Trinity Biomedical Science Institute, 152-160 Pearse Street, Dublin 2, Ireland. Comparative Immunology Group, School of Biochemistry and Immunology, Trinity College Dublin, Trinity Biomedical Science Institute, 152-160 Pearse Street, Dublin 2, Ireland. Department of GU Medicine & Infectious Diseases, St. James's Hospital, Dublin 8, Ireland. Natural Killer Cell Research Group, School of Biochemistry and Immunology, Trinity College Dublin, Trinity Biomedical Science Institute, 152-160 Pearse Street, Dublin 2, Ireland. Electronic address: clair.gardiner@tcd.ie. .
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16: Title: Regulation of interferon lambda-1 (IFNL1/IFN-λ1/IL-29) expression in human colon epithelial cells.
Authors: Swider, Adam, et.al. .
Journal: Cytokine, Vol. 65 (1): 17-23, 2014 .
Snippet: The lambda interferons (comprising three ligands: IFNL1, L2 and L3 - the so-called "Type III" interferons) constitute the most recently discovered IFN family and are known to be important in intestinal anti-viral defense.
Affiliation: Genetic Immunology Laboratory, HUMIGEN LLC, 2439 Kuser Road, Hamilton, NJ 08690, United States(1). .
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17: Title: Different effects of three interferons L on Toll-like receptor-related gene expression in HepG2 cells.
Authors: Kanda, Tatsuo, et.al. .
Journal: Cytokine, Vol. 64 (2): 577-83, 2013 .
Snippet: The effects of IFNL1, IFNL2 and IFNL3 on innate immunity including Toll-like receptor (TLR)-related pathway in human hepatocytes were examined.
Affiliation: Department of Gastroenterology and Nephrology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8677, Japan. Electronic address: kandat-cib@umin.ac.jp. .
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18: Title: Cutting edge: Ku70 is a novel cytosolic DNA sensor that induces type III rather than type I IFN.
Authors: Zhang, Xing, et.al. .
Journal: Journal of immunology (Baltimore, Md. : 1950) (J Immunol), Vol. 186 (8): 4541-5, 2011 .
Snippet: The functional analysis of IFNL1 promoter revealed that positive-regulatory domain I and IFN-stimulated response element sites are predominantly involved in the DNA-mediated IFNL1 activation.
Affiliation: Applied and Developmental Research Directorate, Science Applications International Corporation-Frederick, Inc., National Cancer Institute at Frederick, Frederick, MD 21702, USA. .
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