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    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Avicenna J Med Biotech</journal-id>
      <journal-id journal-id-type="publisher-id">arij002</journal-id>
      <journal-title-group>
        <journal-title>Avicenna Journal of Medical Biotechnology</journal-title>
      </journal-title-group>
      <issn pub-type="ppub">2008-2835</issn>
      <issn pub-type="epub">2008-4625</issn>
      <publisher>
        <publisher-name>Avicenna Research Institute</publisher-name>
      </publisher>
    </journal-meta>

    <article-meta>
      <article-id pub-id-type="publisher-id">ajmb314</article-id>
      <article-id pub-id-type="doi"></article-id>
      <article-id pub-id-type="pmid"></article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
             <subject></subject> 
        </subj-group>
        <subj-group>
            <subject></subject>
        </subj-group> 
      </article-categories>
      <title-group>
        <article-title>Alternative Splicing Generates Different 5&#39; UTRs in OCT4B Variants</article-title>
      </title-group>
        <contrib-group><contrib contrib-type="author"><name><surname>Poursani</surname><given-names>Ensieh M.</given-names></name></contrib><aff>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</aff></contrib-group><contrib-group><contrib contrib-type="author"><name><surname>Mehravar</surname><given-names>Majid</given-names></name></contrib><aff>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</aff></contrib-group><contrib-group><contrib contrib-type="author"><name><surname>Shahryari</surname><given-names>Alireza</given-names></name></contrib><aff>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</aff></contrib-group><contrib-group><contrib contrib-type="author"><name><surname>Mowla</surname><given-names>Seyed Javad</given-names></name></contrib><aff>Molecular Immunology Research Center, Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</aff></contrib-group><contrib-group><contrib contrib-type="author"><name><surname>Mohammad Soltani</surname><given-names>Bahram</given-names></name></contrib><aff>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</aff></contrib-group>
      <pub-date pub-type="ppub">
        <day></day>
        <month></month>
        <year></year>
      </pub-date>
      <pub-date pub-type="epub">
        <day></day>
        <month></month>
        <year></year>
      </pub-date>
      <volume>9</volume>
      <issue>4</issue>
      <fpage>201</fpage>
      <lpage>204</lpage>
      <history>
        <date date-type="received">
          <day>23</day>
          <month>7</month>
          <year>2016</year>
        </date>
        <date date-type="accepted">
          <day>16</day>
          <month>11</month>
          <year>2016</year>
        </date>
      </history>
      <abstract>
      <p>
      &lt;p&gt;Background: The human &lt;em&gt;OCT4&lt;/em&gt; gene, responsible for pluripotency and self-renewal of Embryonic Stem (ES) and Embryonic Carcinoma (EC) cells, can generate several tran-scripts (OCT4A, OCT4B-variant 2, OCT4B-variant 3, OCT4B-variant 5, OCT4B1, OCT4 B2 and OCT4B3) by alternative splicing and alternative promoters. OCT4A that is responsible for ES and EC cell stemness properties is transcribed from a promoter upstream of Exon1a in those cells. The OCT4B group variants (OCT4B-variant2, OCT4B-variant3, OCT4B-variant5, OCT4B1, OCT4B2 and OCT4B3) are transcribed from a different promoter located in intron 1 and some of them respond to the cell stresses, but cannot sustain the ES/EC cell self-renewal. However, the exact function of OCT4B group variants is still unclear.&lt;br /&gt;
Methods: In the present study, we employed RT-PCR and sequencing approaches to explore different forms of &lt;em&gt;OCT4&lt;/em&gt; transcripts.&lt;br /&gt;
Results: Our data revealed that the OCT4B group variants (OCT4B-variant2, OCT4 B-variant3, OCT4B1, OCT4B2 and OCT4B3) have longer 5&amp;#39; UTR in the human bladder carcinoma cell line of 5637.&lt;br /&gt;
Conclusion: These &lt;em&gt;OCT4&lt;/em&gt; variants undergo alternative splicing in their 5&amp;#39; UTR which might exert regulatory roles in transcription and translation mechanisms.&lt;/p&gt;

      </p>
      </abstract>
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