Selected article for: "immune response and STAT1 protein"
Author: Zhao, Yinghua; Sui, Liyan; Wu, Ping; Wang, Wenfang; Wang, Zedong; Yu, Yang; Hou, Zhijun; Tan, Guangyun; Liu, Quan; Wang, Guoqing
Title: A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response
  • Cord-id: f38rxl3j
  • Document date: 2021_9_1
    • ID: f38rxl3j
    Snippet: The recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative agent of ongoing global pandemic of COVID-19, may trigger immunosuppression in the early stage and overactive immune response in the late stage of infection; However, the underlying mechanisms are not well understood. Here we demonstrated that the SARS-CoV-2 nucleocapsid (N) protein dually regulated innate immune responses, i.e., the low-dose N protein suppressed type I interferon (IFN-I) si
    Document: The recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative agent of ongoing global pandemic of COVID-19, may trigger immunosuppression in the early stage and overactive immune response in the late stage of infection; However, the underlying mechanisms are not well understood. Here we demonstrated that the SARS-CoV-2 nucleocapsid (N) protein dually regulated innate immune responses, i.e., the low-dose N protein suppressed type I interferon (IFN-I) signaling and inflammatory cytokines, whereas high-dose N protein promoted IFN-I signaling and inflammatory cytokines. Mechanistically, the SARS-CoV-2 N protein dually regulated the phosphorylation and nuclear translocation of IRF3, STAT1, and STAT2. Additionally, low-dose N protein combined with TRIM25 could suppress the ubiquitination and activation of retinoic acid-inducible gene I (RIG-I). Our findings revealed a regulatory mechanism of innate immune responses by the SARS-CoV-2 N protein, which would contribute to understanding the pathogenesis of SARS-CoV-2 and other SARS-like coronaviruses, and development of more effective strategies for controlling COVID-19.

    Search related documents:
    Co phrase search for related documents
    • acute ards respiratory distress syndrome and luciferase reporter: 1, 2, 3, 4
    • acute ards respiratory distress syndrome and luciferase reporter assay: 1, 2
    • acute ards respiratory distress syndrome and lung carcinoma: 1
    • acute ards respiratory distress syndrome and lung disease: 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73
    • loading control and luciferase reporter: 1, 2, 3
    • loading control and luciferase reporter assay: 1, 2
    • loading control and luciferase reporter plasmid: 1
    • loading control and lysis buffer: 1, 2, 3, 4, 5
    • low binding and lung carcinoma: 1
    • low binding and lung carcinoma cell: 1
    • low binding and lung disease: 1, 2
    • luciferase reporter and lung carcinoma: 1, 2
    • luciferase reporter and lung carcinoma cell: 1, 2
    • luciferase reporter and lung disease: 1, 2, 3, 4, 5
    • luciferase reporter and lysis buffer: 1, 2, 3, 4, 5, 6, 7, 8
    • luciferase reporter assay and lung carcinoma: 1
    • luciferase reporter assay and lung carcinoma cell: 1
    • luciferase reporter assay and lung disease: 1, 2
    • luciferase reporter assay and lysis buffer: 1, 2, 3, 4, 5, 6