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  1. Article ; Online: The Aryl Hydrocarbon Receptor as a Modulator of Anti-viral Immunity.

    Torti, Maria Florencia / Giovannoni, Federico / Quintana, Francisco Javier / García, Cybele Carina

    Frontiers in immunology

    2021  Volume 12, Page(s) 624293

    Abstract: The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which interacts with a wide range of organic molecules of endogenous and exogenous origin, including environmental pollutants, tryptophan metabolites, and microbial ... ...

    Abstract The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which interacts with a wide range of organic molecules of endogenous and exogenous origin, including environmental pollutants, tryptophan metabolites, and microbial metabolites. The activation of AHR by these agonists drives its translocation into the nucleus where it controls the expression of a large number of target genes that include the AHR repressor (AHRR), detoxifying monooxygenases (CYP1A1 and CYP1B1), and cytokines. Recent advances reveal that AHR signaling modulates aspects of the intrinsic, innate and adaptive immune response to diverse microorganisms. This review will focus on the increasing evidence supporting a role for AHR as a modulator of the host response to viral infection.
    MeSH term(s) Active Transport, Cell Nucleus ; Adaptive Immunity ; Animals ; Gene Expression Regulation ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Ligands ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction ; Virus Diseases/genetics ; Virus Diseases/immunology ; Virus Diseases/metabolism ; Virus Diseases/virology ; Viruses/genetics ; Viruses/immunology ; Viruses/pathogenicity
    Chemical Substances Ligands ; Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2021-03-05
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.624293
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Modulation of the Aryl Hydrocarbon Receptor Signaling Pathway Impacts on Junín Virus Replication.

    Pelaez, Miguel Angel / Torti, María Florencia / Alvarez De Lauro, Aaron Ezequiel / Marquez, Agostina Belén / Giovannoni, Federico / Damonte, Elsa Beatriz / García, Cybele Carina

    Viruses

    2023  Volume 15, Issue 2

    Abstract: Junín virus (JUNV), a member of the ... ...

    Abstract Junín virus (JUNV), a member of the family
    MeSH term(s) Animals ; Humans ; Arenaviridae ; Argentina ; Junin virus ; Mammals ; Receptors, Aryl Hydrocarbon/genetics ; Signal Transduction ; Virus Replication
    Chemical Substances Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2023-01-28
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v15020369
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Dengue virus targets RBM10 deregulating host cell splicing and innate immune response.

    Pozzi, Berta / Bragado, Laureano / Mammi, Pablo / Torti, María Florencia / Gaioli, Nicolás / Gebhard, Leopoldo G / García Solá, Martín E / Vaz-Drago, Rita / Iglesias, Néstor G / García, Cybele C / Gamarnik, Andrea V / Srebrow, Anabella

    Nucleic acids research

    2020  Volume 48, Issue 12, Page(s) 6824–6838

    Abstract: RNA-seq experiments previously performed by our laboratories showed enrichment in intronic sequences and alterations in alternative splicing in dengue-infected human cells. The transcript of the SAT1 gene, of well-known antiviral action, displayed higher ...

    Abstract RNA-seq experiments previously performed by our laboratories showed enrichment in intronic sequences and alterations in alternative splicing in dengue-infected human cells. The transcript of the SAT1 gene, of well-known antiviral action, displayed higher inclusion of exon 4 in infected cells, leading to an mRNA isoform that is degraded by non-sense mediated decay. SAT1 is a spermidine/spermine acetyl-transferase enzyme that decreases the reservoir of cellular polyamines, limiting viral replication. Delving into the molecular mechanism underlying SAT1 pre-mRNA splicing changes upon viral infection, we observed lower protein levels of RBM10, a splicing factor responsible for SAT1 exon 4 skipping. We found that the dengue polymerase NS5 interacts with RBM10 and its sole expression triggers RBM10 proteasome-mediated degradation. RBM10 over-expression in infected cells prevents SAT1 splicing changes and limits viral replication, while its knock-down enhances the splicing switch and also benefits viral replication, revealing an anti-viral role for RBM10. Consistently, RBM10 depletion attenuates expression of interferon and pro-inflammatory cytokines. In particular, we found that RBM10 interacts with viral RNA and RIG-I, and even promotes the ubiquitination of the latter, a crucial step for its activation. We propose RBM10 fulfills diverse pro-inflammatory, anti-viral tasks, besides its well-documented role in splicing regulation of apoptotic genes.
    MeSH term(s) Acetyltransferases/genetics ; Alternative Splicing/genetics ; Apoptosis/genetics ; Dengue/genetics ; Dengue/virology ; Dengue Virus/genetics ; Dengue Virus/pathogenicity ; Exons/genetics ; HEK293 Cells ; Host-Pathogen Interactions/genetics ; Humans ; Immunity, Innate/genetics ; Protein Isoforms/genetics ; RNA Splicing/genetics ; RNA-Binding Proteins/genetics ; RNA-Seq ; Virus Replication/genetics
    Chemical Substances Protein Isoforms ; RBM10 protein, human ; RNA-Binding Proteins ; Acetyltransferases (EC 2.3.1.-) ; diamine N-acetyltransferase (EC 2.3.1.57)
    Language English
    Publishing date 2020-05-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkaa340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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