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                <identifier>oai:data.mendeley.com/7nfg4tffs8.1</identifier>
                <datestamp>2022-11-17T14:38:39Z</datestamp>
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            <metadata><oai_dc:dc xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <dc:creator>Zhou, Hong</dc:creator>
    <dc:title>Nucleolin is a Critical Regulator for Primary Transcripts of miR-31 to be a Peptide or an miRNA</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>A study to investigate the role of nucleolin in the regulation of pri-miR-31 to be a peptide or an miRNA. During the activation of CD4+ T cells, the localization of pri-miR-31 shifts from cytoplasm into nucleus, consistent with increasing miR-31 expression and reduced miPEP31, the encoded product of pri-miR-31. We identified nucleolin as the regulator of pri-miR-31. The RNA binding domain of nucleolin interacts with pri-miR-31 through recognizing a G-quadruplex structure. Furthermore, nucleolin binds to a subset of G-quadruplex containing pri-miRNAs, subsequently regulating metabolic reprogramming and activation of CD4+ T cells. After screening endogenous RNA aptamers targeting nucleolin, we found that rG215 relieves the development of experimental colitis via inhibiting the pathogenic CD4+ T cells. Collectively, our results identified nucleolin as a critical regulator of the fate determination of pri-miRNAs and provided a new potential strategy to treat autoimmune diseases.</dc:description>
    <dc:subject>RNA</dc:subject>
    <dc:subject>Immune Regulation</dc:subject>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/7nfg4tffs8.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/7nfg4tffs8.1</dc:identifier>
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    <dc:date>2022-11-17T14:38:39Z</dc:date>
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