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   <ui>gb-spotlight-20000912-01</ui>
   <ji>GBJ</ji>
   <fm>
      <dochead>Research news</dochead>
      <bibl>
         <title>
            <p>MODY-fying gene expression in diabetes</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Weitzman</snm>
               <mi>B</mi>
               <fnm>Jonathan</fnm>
               <email>JWeitzman@elabseurope.com</email>
            </au>
         </aug>
         <source>Genome Biology</source>
         <issn>1465-6906</issn>
         <pubdate>2000</pubdate>
         <volume>1</volume>
         <fpage>spotlight-20000912-01</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/gb-spotlight-20000912-01</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>12</day>
               <month>09</month>
               <year>2000</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2000</year>
         <collab>BioMed Central Ltd</collab>
      </cpyrt>
      <shortabs>
         <p>Identification of genes that are regulated by the transcription factor HNF1alpha may explain its involvement in MODY3 diabetes.</p>
      </shortabs>
   </fm>
   <meta>
      <classifications>
         <classification type="STATUS">Archive</classification>
      </classifications>
   </meta>
   <bdy>
      <sec>
         <st>
            <p/>
         </st>
         <p>HNF1&#945; (hepatocyte nuclear factor 1) was originally isolated as a liver transcription factor. So it came as a sweet surprise to researchers when HNF1&#945; was identified as the gene mutated in patients suffering from <abbr bid="B1">MODY3, maturity onset diabetes of the young subtype 3</abbr>. As they report in the 15 August <abbr bid="B2"><it>EMBO Journal</it></abbr> Wang <it>et al</it>. (<it>EMBO Journal</it> 2000, <b>19</b>:4257-4264) used a <abbr bid="B3">tetracyclin-regulated</abbr> system to identify genes controlled by HNF1&#945;. They expressed the most common diabetes-associated mutant form of HNF1&#945; (P291fsinsC) in the INS-1 insulinoma cell line. This mutant form reduced the expression of several genes important for pancreatic &#946;-cell function and inhibited expression of the insulin gene. Other genes suppressed by HNF1&#945; include those involved in glucose transport (GLUT2) and glycolysis (e.g. encoding proteins aldolase B and L-pyruvate kinase). These inhibitory effects result in reduced cellular insulin, insulin secretion and ATP production.</p>
      </sec>
   </bdy>
   <bm>
      <refgrp>
         <bibl id="B1">
            <note>Mutations in the hepatocyte nuclear factor-1alpha gene in maturity-onset diabetes of the young. </note>
            <xrefbib>
               <pubid idtype="pmpid">8945470</pubid>
            </xrefbib>
         </bibl>
         <bibl id="B2">
            <url>http://www.emboj.org/</url>
            <note>EMBO Journal</note>
         </bibl>
         <bibl id="B3">
            <note>Transcriptional activation by tetracyclines in mammalian cells. </note>
            <xrefbib>
               <pubid idtype="pmpid">7792603</pubid>
            </xrefbib>
         </bibl>
      </refgrp>
   </bm>
</art>
