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Yersinia YopT inhibits RLH-mediated NF-kappa B and IRF3 signal transduction

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单位: [1]Bioengineering, college of Biological Engineering and Food, Hubei University of Technology, P.R. China. [2]Beijing Institute of Biotechnology, Beijing, P.R. China. [3]Clinical Laboratory Center, Beijing Friendship Hospital, Capital Medical University, Beijing, P.R. China. [4]Department of Gastroenterology and Hepatology, the Fifth Medical Center of Chinese PLA General Hospital, Beijing, P.R. China [5]Beijing Key Laboratory of POCT for Bioemergency and Clinic (No. BZ0329), [6]Beijing Hotgen Biotechnology Inc., Beijing 100071, P. R. China [7]These authors contributed equally to this work
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关键词: IFN regulatory factor-3 nuclear factor-kappa B rat liver homogenate YersiniaYopT

摘要:
The Gram-negative bacterial pathogenYersiniadelivers six effector proteins into the host cells to block the host innate immune response. One of the effectors, YopT, is a potent cysteine protease that causes the disruption of the actin cytoskeleton to inhibit phagocytosis of the pathogen; however, its molecular mechanism and relevance to pathogenesis need further investigation. In this report, we show that RIG-I is a novel target of the YopT protein. Remarkably, YopT interacts with RIG-I and inhibits rat liver homogenate-mediated nuclear factor-kappa B and interferon regulatory factor-3 activation. Further studies revealed a YopT-dependent increase in the K48-polymerized ubiquitination of RIG-I. These findings suggest that YopT negatively regulates RIG-I-mediated cellular antibacterial response by targeting RIG-I.

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出版当年[2019]版:
大类 | 4 区 医学
小类 | 4 区 免疫学 4 区 微生物学
最新[2025]版:
大类 | 4 区 医学
小类 | 4 区 免疫学 4 区 微生物学
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出版当年[2018]版:
Q4 IMMUNOLOGY Q4 MICROBIOLOGY
最新[2024]版:
Q4 IMMUNOLOGY Q4 MICROBIOLOGY

影响因子: 最新[2024版] 最新五年平均[2021-2025] 出版当年[2018版] 出版当年五年平均[2014-2018] 出版前一年[2017版] 出版后一年[2019版]

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第一作者单位: [1]Bioengineering, college of Biological Engineering and Food, Hubei University of Technology, P.R. China. [2]Beijing Institute of Biotechnology, Beijing, P.R. China. [7]These authors contributed equally to this work
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通讯机构: [1]Bioengineering, college of Biological Engineering and Food, Hubei University of Technology, P.R. China. [7]These authors contributed equally to this work
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