LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 3 of total 3

Search options

  1. Article ; Online: Deacetylase Sirtuin 1 mitigates type I IFN- and type II IFN-induced signaling and antiviral immunity.

    Yu, Shuang-Shuang / Tang, Rong-Chun / Zhang, Ao / Geng, Shijin / Yu, Hengxiang / Zhang, Yan / Sun, Xiu-Yuan / Zhang, Jun

    Journal of virology

    2024  Volume 98, Issue 3, Page(s) e0008824

    Abstract: Type I and type II IFNs are important immune modulators in both innate and adaptive immunity. They transmit signaling by activating JAK-STAT pathways. Sirtuin 1 (SIRT1), a class III ... ...

    Abstract Type I and type II IFNs are important immune modulators in both innate and adaptive immunity. They transmit signaling by activating JAK-STAT pathways. Sirtuin 1 (SIRT1), a class III NAD
    MeSH term(s) Animals ; Mice ; Immunity, Innate ; Interferon Type I/metabolism ; Interferon-gamma ; Phosphorylation ; Signal Transduction ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; STAT1 Transcription Factor/metabolism ; Virus Diseases/immunology
    Chemical Substances Interferon Type I ; Interferon-gamma (82115-62-6) ; Sirtuin 1 (EC 3.5.1.-) ; STAT1 Transcription Factor ; Sirt1 protein, mouse (EC 3.5.1.-)
    Language English
    Publishing date 2024-02-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.00088-24
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Deubiquitinase USP47 attenuates virus-induced type I interferon signaling.

    Chen, Hong-Yan / Tang, Rong-Chun / Liang, Jia-Wei / Zhao, Weijia / Yu, Shuang-Shuang / Yao, Ran-Ran / Xu, Rui / Zhang, Ao / Geng, Shijin / Sun, Xiu-Yuan / Ge, Qing / Zhang, Jun

    International immunopharmacology

    2023  Volume 118, Page(s) 110040

    Abstract: The innate immune responses are tightly regulated to ensure effective clearance of invading pathogens and avoid excessive inflammation. Ubiquitination and deubiquitination are important post-translational modifications in antiviral immune responses. Here, ...

    Abstract The innate immune responses are tightly regulated to ensure effective clearance of invading pathogens and avoid excessive inflammation. Ubiquitination and deubiquitination are important post-translational modifications in antiviral immune responses. Here, we discovered deubiquitinase USP47 as a novel negative immune system regulator. Overexpression of USP47 repressed Sendai virus, poly(I:C) and poly(dA:dT)-induced ISRE and IFN-β activation, along with reduced IFNB1 transcription and enhanced viral replication. Knockdown of USP47 expression had the opposite effects. Dual-luciferase and phosphorylation assays showed that USP47 targeted downstream of MAVS and upstream of TBK1. Additional co-immunoprecipitation assays suggested that USP47 interacted with TRAF3 and TRAF6. Importantly, USP47 removed K63-linked polyubiquitin chains from TRAF3 and TRAF6. Hence, we describe a novel modulator of the antiviral innate immune response, USP47, which removes K63-linked polyubiquitins from TRAF3 and TRAF6, leading to reduced type I IFN signaling.
    MeSH term(s) TNF Receptor-Associated Factor 3/genetics ; TNF Receptor-Associated Factor 3/metabolism ; TNF Receptor-Associated Factor 6/metabolism ; Immunity, Innate ; Interferon Type I/metabolism ; Antiviral Agents ; Viruses ; Ubiquitination ; Deubiquitinating Enzymes/metabolism
    Chemical Substances TNF Receptor-Associated Factor 3 ; TNF Receptor-Associated Factor 6 ; Interferon Type I ; Antiviral Agents ; Deubiquitinating Enzymes (EC 3.4.19.12)
    Language English
    Publishing date 2023-03-29
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.110040
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5408: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation.

    Xu, Rui / Yu, Shuang-Shuang / Yao, Ran-Ran / Tang, Rong-Chun / Liang, Jia-Wei / Pang, Xuewen / Zhang, Jun

    Frontiers in immunology

    2021  Volume 12, Page(s) 755512

    Abstract: Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and ...

    Abstract Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and the acting mechanisms of LINC02605 in antiviral innate immune response. LINC02605 was up-regulated by RNA virus, DNA virus, and type I IFNs in NF-κB and Jak-stat dependent manner. Overexpression of LINC02605 promotes RNA virus-induced type I interferon production and inhibited viral replication. Consistently, knockdown of LINC02605 resulted in reduced antiviral immune response and increased viral replication. Mechanistically, LINC02605 released the inhibition of hsa-miR-107 on the expression of phosphatase and tensin homolog (PTEN). By microRNA mimics and inhibitors, hsa-miR-107 was demonstrated to not only inhibit PTEN's expression but also negatively regulate the antiviral immune response. Knockdown of LINC02605 led to the reduction of PTEN expression both in mRNA and protein levels. Overexpression of LINC02605 had an opposite impact. Moreover, LINC02605 attenuated the serine 97 phosphorylation level of interferon regulatory factor 3 (IRF3) by promoting PTEN expression. Nucleoplasmic fragmentation assay showed that knocking down LINC02605 inhibited the nuclear translocation of IRF3, rendering the host cells more susceptible to viral invasion, while overexpression showed opposite effects. Therefore, LINC02605 is an induced lncRNA by viral infection and plays a positive feedback in antiviral immune response through modulating the nuclear translocation of IRF3.
    MeSH term(s) Active Transport, Cell Nucleus/immunology ; Cell Line ; Gene Expression Regulation/immunology ; Humans ; Immunity, Innate/immunology ; Interferon Regulatory Factor-3/immunology ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/immunology ; MicroRNAs/immunology ; RNA, Long Noncoding/immunology ; Virus Diseases/immunology
    Chemical Substances IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interferon Type I ; MIRN107 microRNA, human ; MicroRNAs ; RNA, Long Noncoding
    Language English
    Publishing date 2021-11-05
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.755512
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top