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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Coronavirus</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Dominio científico: Coronavirus</text>
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    <name>Text</name>
    <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-β in Porcine Intestinal Epithelial Cells</text>
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          <name>Creator</name>
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              <text>Shaoju Qian, Zi-tong Gao, Rui Cao, Kang Yang, Yijie Cui, Shaowen Li, Xianrong Meng, Qigai He, Zili Li</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>Transmissible gastroenteritis virus (TGEV) is a porcine intestinal coronavirus that causes fatal severe watery diarrhea in piglets. The neonatal Fc receptor (FcRn) is the only IgG transport receptor, its expression on mucosal surfaces is triggered upon viral stimulation, which significantly enhances mucosal immunity. We utilized TGEV as a model pathogen to explore the role of FcRn in resisting viral invasion in overall intestinal mucosal immunity. TGEV induced FcRn expression by activating NF-κB signaling in porcine small intestinal epithelial (IPEC-J2) cells, however, the underlying mechanisms are unclear. First, using small interfering RNAs, we found that TGEV up-regulated FcRn expression via TLR3, TLR9 and RIG-I. Moreover, TGEV induced IL-1β, IL-6, IL-8, TGF-β, and TNF-α production. TGF-β-stimulated IPEC-J2 cells highly up-regulated FcRn expression, while treatment with a JNK-specific inhibitor down-regulated the expression. TGEV nucleocapsid (N) protein also enhanced FcRn promoter activity via the NF-κB signaling pathway and its central region (aa 128–252) was essential for FcRn activation. Additionally, N protein-mediated FcRn up-regulation promotes IgG transcytosis. Thus, TGEV N protein and TGF-β up-regulated FcRn expression, further clarifying the molecular mechanism of up-regulation of FcRn expression by TGEV.</text>
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          <name>Date</name>
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              <text>2020</text>
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          <name>Subject</name>
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              <text>Transmissible gastroenteritis virus, Nucleocapsid protein, TGF-β, neonatal Fc receptor, toll-like receptor, NF-κB</text>
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          <name>Identifier</name>
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              <text>DOI: 10.3389/fmicb.2019.03085</text>
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          <name>Source</name>
          <description>A related resource from which the described resource is derived</description>
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            <elementText elementTextId="13030">
              <text>Frontiers in Microbiology</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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              <text>Frontiers Media S.A.</text>
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          <name>Coverage</name>
          <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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              <text>Microbiology</text>
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          <name>Language</name>
          <description>A language of the resource</description>
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              <text>EN</text>
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