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J. Biol. Chem., Vol. 283, Issue 37, 25617-25627, September 12, 2008

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CAATT/Enhancer-binding Proteins and Interact with NKX2-1 to Synergistically Activate Mouse Secretoglobin 3A2 Gene Expression^*

Takeshi Tomita¹, Taketomo Kido, Reiko Kurotani, Shun-ichiro Iemura^¶, Esta Sterneck^||, Tohru Natsume^¶, Charles Vinson, and Shioko Kimura²

From the Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892, the Cardiovascular Research Institute, Yokohama City University, Yokohama 236-0006, Japan, the ^¶National Institutes of Advanced Industrial Science and Technology, Biological Information Research Center, Tokyo 135-0064, Japan, and the ^||Laboratory of Cell and Developmental Signaling, NCI, Frederick, Maryland 21702-1201

Secretoglobin (SCGB) 3A2 is a small molecular weight secreted protein predominantly expressed in lung airways. We previously demonstrated that the expression of SCGB3A2 is regulated by homeodomain transcription factor NKX2-1. Here we show that CCAAT/enhancer-binding proteins, C/EBP and C/EBP, regulate mouse Scgb3a2 gene transcription in vivo and in vitro by binding to specific sites located in the Scgb3a2 promoter and the activity is synergistically enhanced through cooperative interaction with NKX2-1. Six C/EBP binding sites lie within 500 bp of the Scgb3a2 gene promoter, of which two sites, located at -44 to -54 bp and -192 to -201 bp, appear to be critical for the synergistic activation of Scgb3a2 gene transcription with NKX2-1. All three transcription factors, C/EBP, C/EBP, and NKX2-1, are expressed in the epithelial cells of airways, particularly the bronchus, where high expression of SCGB3A2 is found. The expression of these transcription factors markedly increases toward the end of gestation, which coincides with the marked increase of SCGB3A2, suggesting the importance of C/EBP and C/EBP, and their synergistic interaction with NKX2-1 in mouse Scgb3a2 gene transcription and lung development.

Received for publication, July 7, 2008 , and in revised form, July 16, 2008.

^* This work was authored, in whole or in part, by National Institutes of Health staff. This work was supported by the Intramural Research Program of the National Cancer Institute, Center for Cancer Research, and in part by the New Energy and Industrial Technology Development Organization (to T. N.). 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental data, references, and Table S1.

¹ Present address: Dept. of Pharmacology, Tokyo Women's Medical University, Tokyo 162-8666, Japan.

² To whom correspondence should be addressed: Bldg. 37, Rm. 3112B, National Institutes of Health, Bethesda, MD 20892. Tel.: 301-496-0958; Fax: 301-496-8419; E-mail: kimuras{at}mail.nih.gov.

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