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      <src>https://socictopen.socict.org/files/original/4789b952f325ca653597f18872ce584d.pdf</src>
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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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        <element elementId="50">
          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Coronavirus infection, ER stress and Apoptosis</text>
            </elementText>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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            <elementText elementTextId="7932">
              <text>TO SING eFUNG, Ding Xiang eLiu</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>The replication of coronavirus, a family of important animal and human pathogens, is closely associated with the cellular membrane compartments, especially the endoplasmic reticulum (ER). Coronavirus infection of cultured cells was previously shown to cause ER stress and induce the unfolded protein response (UPR), a process that aims to restore the ER homeostasis by global translation shutdown and increasing the ER folding capacity. However under prolonged ER stress, UPR can also induce apoptotic cell death. Accumulating evidence from recent studies has shown that induction of ER stress and UPR may constitute a major aspect of coronavirus-host interaction. Activation of the three branches of UPR modulates a wide variety of signaling pathways, such as mitogen-activated protein (MAP) kinases activation, autophagy, apoptosis and innate immune response.  ER stress and UPR activation may therefore contribute significantly to the viral replication and pathogenesis during coronavirus infection. In this review, we summarize current knowledge on coronavirus-induced ER stress and UPR activation, with emphasis on their cross-talking to apoptotic signaling.</text>
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              <text>2014</text>
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          <name>Subject</name>
          <description>The topic of the resource</description>
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              <text>apoptosis, coronavirus, Unfolded Protein Response, ER stress, signal transduction pathways, Proinflammatory cytokines</text>
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          <name>Identifier</name>
          <description>An unambiguous reference to the resource within a given context</description>
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              <text>DOI: 10.3389/fmicb.2014.00296</text>
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          <name>Source</name>
          <description>A related resource from which the described resource is derived</description>
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              <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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            <elementText elementTextId="7938">
              <text>Frontiers Media S.A.</text>
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          </elementTextContainer>
        </element>
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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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            <elementText elementTextId="7939">
              <text>Microbiology</text>
            </elementText>
          </elementTextContainer>
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          <name>Language</name>
          <description>A language of the resource</description>
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            <elementText elementTextId="7940">
              <text>EN</text>
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