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J. Biol. Chem., Vol. 280, Issue 3, 1893-1900, January 21, 2005

This Article Full Text Full Text (PDF) All Versions of this Article: 280/3/1893    most recent M410759200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hashimoto, T. Articles by Kashiwagi, A. Search for Related Content PubMed PubMed Citation Articles by Hashimoto, T. Articles by Kashiwagi, A. Social Bookmarking                      What's this?

Regulation of ATP-sensitive Potassium Channel Subunit Kir6.2 Expression in Rat Intestinal Insulin-producing Progenitor Cells^*

Tetsuya Hashimoto, Takaaki Nakamura, Hiroshi Maegawa, Yoshihiko Nishio, Katsuya Egawa, and Atsunori Kashiwagi¶

From the Division of Endocrinology and Metabolism, Department of Medicine, and the Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, 520-2192, Japan

We have reported that the combined expression of Pdx-1 (pancreatic duodenal homeobox 1) and Isl-1 (islet 1) enables immature rat enterocytes (IEC-6) to produce and release insulin. A key component regulating the release of insulin is the ATP-sensitive potassium channel subunit Kir6.2. To investigate the regulation of Kir6.2 gene expression, we assessed Kir6.2 expression in IEC-6 cells expressing Pdx-1 and/or Isl-1. We observed that Kir6.2 protein was expressed de novo in IEC-6 cells expressing both Pdx-1 and Isl-1 but not in cells expressing Pdx-1 alone. Next, we analyzed the regions of the Kir6.2 promoter (–1677/–45) by performing a luciferase assay and electrophoretic mobility shift assay. The results have demonstrated that Kir6.2 promoter possesses two regions regulating the promoter activity: a Foxa2-binding site (–1364 to –1210) and an Sp1/Sp3-binding site (–1035 to –939). The additional expression of Isl-1 in IEC-6 cells expressing Pdx-1 attenuated overexpression of Foxa2 protein and enhanced Kir6.2 expression. Finally, knockdown of Isl-1 using the iRNA technique resulted in decreased expression of Kir6.2 protein in a rat pancreatic -cell line (RIN-5F cells). These results indicate that expression of Kir6.2 in the rat intestine is moderated by Isl-1.

Received for publication, September 20, 2004 , and in revised form, October 28, 2004.

^* This work was supported, in part, by Grant-in-aid for Scientific Research (C) 16590143 from the Ministry of Education, Science and Culture of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom all correspondence should be addressed. Tel.: 81-77-548-2223; Fax: 81-77-543-3858; E-mail: kasiwagi{at}belle.shiga-med.ac.jp.

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