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: FTO Suppresses STAT3 Activation and Modulates Proinflammatory Interferon-Stimulated Gene Expression.

    McFadden, Michael J / Sacco, Matthew T / Murphy, Kristen A / Park, Moonhee / Gokhale, Nandan S / Somfleth, Kim Y / Horner, Stacy M

    Journal of molecular biology

    2021  Volume 434, Issue 6, Page(s) 167247

    Abstract: Signaling initiated by type I interferon (IFN) results in the induction of hundreds of IFN-stimulated genes (ISGs). The type I IFN response is important for antiviral restriction, but aberrant activation of this response can lead to inflammation and ... ...

    Abstract Signaling initiated by type I interferon (IFN) results in the induction of hundreds of IFN-stimulated genes (ISGs). The type I IFN response is important for antiviral restriction, but aberrant activation of this response can lead to inflammation and autoimmunity. Regulation of this response is incompletely understood. We previously reported that the mRNA modification m
    MeSH term(s) Alpha-Ketoglutarate-Dependent Dioxygenase FTO/genetics ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/metabolism ; Gene Expression ; Gene Expression Regulation ; Humans ; Inflammation/genetics ; Interferon Type I/metabolism ; Methyltransferases/metabolism ; RNA, Messenger/genetics ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism
    Chemical Substances Interferon Type I ; RNA, Messenger ; STAT3 Transcription Factor ; STAT3 protein, human ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO (EC 1.14.11.33) ; FTO protein, human (EC 1.14.11.33) ; Methyltransferases (EC 2.1.1.-)
    Language English
    Publishing date 2021-09-16
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80229-3
    ISSN 1089-8638 ; 0022-2836
    ISSN (online) 1089-8638
    ISSN 0022-2836
    DOI 10.1016/j.jmb.2021.167247
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 867: 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: FTO Suppresses STAT3 Activation and Modulates Proinflammatory Interferon-Stimulated Gene Expression

    McFadden, Michael J. / Sacco, Matthew T. / Murphy, Kristen A. / Park, Moonhee / Gokhale, Nandan S. / Somfleth, Kim Y. / Horner, Stacy M.

    Journal of molecular biology. 2021 Sept. 11,

    2021  

    Abstract: Signaling initiated by type I interferon (IFN) results in the induction of hundreds of IFN-stimulated genes (ISGs). The type I IFN response is important for antiviral restriction, but aberrant activation of this response can lead to inflammation and ... ...

    Abstract Signaling initiated by type I interferon (IFN) results in the induction of hundreds of IFN-stimulated genes (ISGs). The type I IFN response is important for antiviral restriction, but aberrant activation of this response can lead to inflammation and autoimmunity. Regulation of this response is incompletely understood. We previously reported that the mRNA modification m⁶A and its deposition enzymes, METTL3 and METTL14 (METTL3/14), promote the type I IFN response by directly modifying the mRNA of a subset of ISGs to enhance their translation. Here, we determined the role of the RNA demethylase fat mass and obesity-associated protein (FTO) in the type I IFN response. FTO, which can remove either m⁶A or cap-adjacent m⁶Am RNA modifications, has previously been associated with obesity and body mass index, type 2 diabetes, cardiovascular disease, and inflammation. We found that FTO suppresses the transcription of a distinct set of ISGs, including many known pro-inflammatory genes, and that this regulation requires its catalytic activity but is not through the actions of FTO on m⁶Am. Interestingly, depletion of FTO led to activation of the transcription factor STAT3, whose role in the type I IFN response is not well understood. This activation of STAT3 increased the expression of a subset of ISGs. Importantly, this increased ISG induction resulting from FTO depletion was partially ablated by depletion of STAT3. Together, these results reveal that FTO negatively regulates STAT3-mediated signaling that induces proinflammatory ISGs during the IFN response, highlighting an important role for FTO in suppression of inflammatory genes.
    Keywords autoimmunity ; body mass index ; cardiovascular diseases ; catalytic activity ; gene expression ; inflammation ; interferons ; molecular biology ; noninsulin-dependent diabetes mellitus ; obesity ; transcription factors
    Language English
    Dates of publication 2021-0911
    Publishing place Elsevier Ltd
    Document type Article
    Note Pre-press version
    ZDB-ID 80229-3
    ISSN 1089-8638 ; 0022-2836
    ISSN (online) 1089-8638
    ISSN 0022-2836
    DOI 10.1016/j.jmb.2021.167247
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

    In stock of ZB MED Bonn / Germany

    Z 4' 63/108: Show issues

    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.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  3. Article ; Online: ADAR1 mutation causes ZBP1-dependent immunopathology.

    Hubbard, Nicholas W / Ames, Joshua M / Maurano, Megan / Chu, Lan H / Somfleth, Kim Y / Gokhale, Nandan S / Werner, Margo / Snyder, Jessica M / Lichauco, Katrina / Savan, Ram / Stetson, Daniel B / Oberst, Andrew

    Nature

    2022  Volume 607, Issue 7920, Page(s) 769–775

    Abstract: The RNA-editing enzyme ADAR1 is essential for the suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA ... ...

    Abstract The RNA-editing enzyme ADAR1 is essential for the suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA species
    MeSH term(s) Adenosine Deaminase/genetics ; Adenosine Deaminase/metabolism ; Animals ; Caspase 8/genetics ; Caspase 8/metabolism ; Cell Death ; Gene Deletion ; Immune System Diseases/genetics ; Immune System Diseases/metabolism ; Immune System Diseases/pathology ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Mammals/genetics ; Mutation ; Protein Kinases/deficiency ; Protein Kinases/genetics ; RNA, Double-Stranded/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/deficiency ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Signal Transduction
    Chemical Substances RNA, Double-Stranded ; RNA-Binding Proteins ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Caspase 8 (EC 3.4.22.-) ; Adenosine Deaminase (EC 3.5.4.4)
    Language English
    Publishing date 2022-07-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-04896-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: 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)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

    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