نتایج جستجو برای: interferon regulatory factor 7 irf7

تعداد نتایج: 1617638  

Journal: :Journal of immunology 2011
Qiming Liang Hongying Deng Xiaojuan Li Xianfang Wu Qiyi Tang Tsung-Hsien Chang Hongzhuang Peng Frank J Rauscher Keiko Ozato Fanxiu Zhu

IFN regulatory factor 7 (IRF7) is a potent transcription factor of type I IFNs and IFN-stimulated genes and is known as the master regulator of type I IFN-dependent immune responses. Because excessive responses could harm the host, IRF7 itself is delicately regulated at the transcriptional, translational, and posttranslational levels. Modification of IRF7 by small ubiquitin-related modifiers (S...

2014
Nilufer Esen Emily K Rainey-Barger Amanda K Huber Pennelope K Blakely David N Irani

Lymphoid chemokines are crucial for the development and maintenance of lymphoid organs, but their ectopic expression in non-lymphoid tissues is implicated in both local response to infection and chronic organ-specific autoimmunity. Production of one such chemokine, C-X-C motif ligand 13 (CXCL13), within the central nervous system (CNS) has been linked to the pathogenesis of multiple sclerosis (...

Journal: :Science 2010
Miwa Sasai Melissa M Linehan Akiko Iwasaki

Endosomal Toll-like receptors (TLRs) 7 and 9 recognize viral pathogens and induce signals leading to the activation of nuclear factor κB (NF-κB)-dependent proinflammatory cytokines and interferon regulatory factor 7 (IRF7)-dependent type I interferons (IFNs). Recognition of viral nucleic acids by TLR9 requires its cleavage in the endolysosomal compartment. Here, we show that TLR9 signals leadin...

2014
Liang-Che Chang Chung-Wei Fan Wen-Ko Tseng Hui-Ping Chein Tsan-Yu Hsieh Jim-Ray Chen Cheng-Cheng Hwang Chung-Ching Hua Chun-xia Cao.

Toll-like receptor (TLR) 9 plays a role in intestinal inflammation that, in turn, is related to the tumorigenesis of colorectal cancer. Nuclear factor κB (NFκB), and interferon regulatory factor (IRF) 5 and IRF7 can be activated by TLR9 and induce the production of proinflammatory cytokines and type I interferon, respectively. This study investigated the mRNA expressions of TLR9 and its downstr...

2012
Pierre Génin Rongtuan Lin John Hiscott Ahmet Civas

BACKGROUND Induction of Type I Interferon (IFN) genes constitutes an essential step leading to innate immune responses during virus infection. Sendai virus (SeV) infection of B lymphoid Namalwa cells transiently induces the transcriptional expression of multiple IFN-A genes. Although transcriptional activation of IFN-A genes has been extensively studied, the mechanism responsible for the attenu...

Journal: :Journal of virology 2014
Jung Sook Ye Nari Kim Kyoung Jin Lee Young Ran Nam Uk Lee Chul Hyun Joo

UNLABELLED Beta interferon (IFN-β) is involved in a wide range of cellular functions, and its secretion must be tightly controlled to inhibit viral spreading while minimizing cellular damage. Intracellular viral replication triggers cellular signaling cascades leading to the activation of the transcription factors NF-κB and interferon regulatory factor 3 (IRF3) and IRF7 (IRF3/7), which synergis...

Journal: :Journal of virology 2009
Eric D Tang Cun-Yu Wang

The innate immune system recognizes nucleic acids during viral infection and stimulates cellular antiviral responses. Intracellular detection of RNA virus infection is mediated by the RNA helicases RIG-I (retinoic acid inducible gene I) and MDA-5, which recognize viral RNA and signal through the adaptor molecule MAVS (mitochondrial antiviral signaling) to stimulate the phosphorylation and activ...

Journal: :Journal of virology 2004
Rongtuan Lin Ryan S Noyce Susan E Collins Roger D Everett Karen L Mossman

Virus infection induces a rapid cellular response in cells characterized by the induction of interferon. While interferon itself does not induce an antiviral response, it activates a number of interferon-stimulated genes that collectively function to inhibit virus replication and spread. Previously, we and others reported that herpes simplex virus type 1 (HSV-1) induces an interferon -independe...

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