<?xml version="1.0" encoding="UTF-8" ?>

    <journal>
    <language>en</language>
    <journal_id_issn>2008-2835</journal_id_issn>
    <journal_id_issn_online>2008-4625</journal_id_issn_online>
    <journal_id_pii></journal_id_pii>
    <journal_id_doi></journal_id_doi>
    <journal_id_isnet></journal_id_isnet>
    <journal_id_iranmedex>276</journal_id_iranmedex>
    <journal_id_magiran>5669</journal_id_magiran>
    <journal_id_sid>11181</journal_id_sid>
    <pubdate>
	    <type>gregorian</type>
	    <year>>2017</year>
	    <month>>October-December</month>
	    <day></day>
    </pubdate>
    <volume>9</volume>
    <number>4</number>
    <publish_type>online</publish_type>
    <publish_edition>1</publish_edition>
    <article_type>fulltext</article_type>
    <articleset>

<article>
	<language>en</language>
	<article_id_issn></article_id_issn>
	<article_id_issn_online></article_id_issn_online>
	<article_id_pubmed>29090070</article_id_pubmed>
	<article_id_pii></article_id_pii>
	<article_id_doi></article_id_doi>
	<article_id_iranmedex></article_id_iranmedex>
	<article_id_magiran></article_id_magiran>
	<article_id_sid></article_id_sid>
	<title_fa></title_fa>
	<title>Alternative Splicing Generates Different 5&#39; UTRs in OCT4B Variants</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>&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;
</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Alternative splicing, Genes, 5’untranslated regions</keyword>
	<start_page>201</start_page>
	<end_page>204</end_page>
	<web_url>https://www.ajmb.org/En/Article.aspx?id=314</web_url>
    <pdf_url>https://www.ajmb.org/PDF/En/FullText/314.pdf</pdf_url>
	<author_list><author><first_name>Ensieh M.</first_name><middle_name></middle_name><last_name>Poursani</last_name><suffix></suffix><affiliation>Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>1139</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Majid</first_name><middle_name></middle_name><last_name>Mehravar</last_name><suffix></suffix><affiliation>Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>1140</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Alireza</first_name><middle_name></middle_name><last_name>Shahryari</last_name><suffix></suffix><affiliation>Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>1259</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Seyed Javad</first_name><middle_name></middle_name><last_name>Mowla</last_name><suffix></suffix><affiliation>Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>248</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Bahram</first_name><middle_name></middle_name><last_name>Mohammad Soltani</last_name><suffix></suffix><affiliation>Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>1141</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author></author_list>
</article>

</articleset>
</journal>

