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            <header>
                <identifier>oai:data.mendeley.com/c2zvxm27yc.1</identifier>
                <datestamp>2019-09-13T08:01:14Z</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>Carino, Adriana</dc:creator>
    <dc:title>Transcriptomic analysis of a mouse model of intrahepatic cholestasis</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>The Farnesoid X receptor (FXR), is the main bile acids sensor expressed in hepatocytes. Obeticholic acid (OCA), a fairly potent FXR agonist, has been approved for the treatment of UDCA-resistant PBC, but FXR gene ablation protects against liver injury in cholestatic modes. The use of OCA causes itching in a substantial proportion of PBC patients, and at the dose 5 mg/d, has been linked to a cluster of severe liver injury, in some cases fatal, in PBC patients with decompensated cirrhosis and Child-Pugh Class B/C. To further elucidate the role of FXR in the pathogenesis of cholestasis, we have tested the obeticholic acid alone or in combination with a FXR antagonist, named as GP7, in a mouse model of ANIT (α-naphthylisothiocyanate) induced cholestasis. OCA and GP7 intrahepatic effect were evaluated by RNAseq analysis performed on Ion S5 Sequencer with Torrent Suite Software v6.</dc:description>
    <dc:subject>Gastroenterology</dc:subject>
    <dc:subject>RNA Sequencing</dc:subject>
    <dc:subject>Cholestasis</dc:subject>
    <dc:contributor>Fiorucci, Stefano</dc:contributor>
    <dc:contributor>Biagioli, Michele</dc:contributor>
    <dc:contributor>Marchianò, Silvia</dc:contributor>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/c2zvxm27yc.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/c2zvxm27yc.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
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    <dc:date>2019-09-13T08:01:14Z</dc:date>
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