## Abstract Hepatic nuclear protein has been reported to bind specifically to the TTGGC sequence of the rat regucalcin gene promoter region in stimulating the promoter activity (Misawa and Yamaguchi [2000] Biochem. Biophys. Res. Commun. 279: 275–281). The present study was undertaken to identify tr
Novel protein RGPR-p117: The gene expression in physiologic state and the binding activity to regucalcin gene promoter region in rat liver
✍ Scribed by Masayoshi Yamaguchi; Hiroyuki Misawa; Zhong Jie Ma
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 223 KB
- Volume
- 88
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
The binding activity of a novel regucalcin gene promoter region‐related protein (RGPR‐p117) to the TTGGC sequence of the rat regucalcin gene promoter region was investigated. The expression of RGPR‐p117 mRNA was seen in the liver tissues of male and female rats. The sexual difference of this expression was not found. Liver RGPR‐p117 mRNA expression was not changed with increasing age (1–50 weeks old), and its expression was not altered by fasting or refeeding. Nuclear factor I‐A1 (NF1‐A1) has been identified to be a transcription factor in stimulating the rat regucalcin gene promoter activity (Misawa and Yamaguchi [2002a] J Cell Biochem 84:795–802]. Recombinant nuclear factor I‐A1 (NF1‐A1) and RGPR‐p117 proteins were used gel mobility shift assay. RGPR‐p117 could not bind to TTGGC motif of the sequence between −525 and −504, which has been defined as a functional promoter element II‐b. NF1‐A1 was specifically bound to the II‐b oligonucleotide. Moreover, RGPR‐p117 was not bound to the II‐b oligonucleotide in the presence of NF1‐A1 or rat liver nuclear protein. The binding of NF1‐A1 to the II‐b oligonucleotide was not altered in the presence of RGPR‐p117. This study demonstrates that RGPR‐p117 mRNA, is expressed stably for physiologic change in rat liver, and that recombinant the protein does not directly bind to the TTGGC motif in rat regucalcin gene promoter. J. Cell. Biochem. 88: 1092–1100, 2003. © 2003 Wiley‐Liss, Inc.
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