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肝脏富集反式作用因子DBP和HNF1在人胰岛素样生长因子结合蛋白-1(IGFBP-1)启动子反式激活中的相互作用

Interplay of the liver-enriched trans-acting factors, DBP and HNF1, in the transactivation of human IGFBP-1 promoter.

作者信息

Babajko S, Groyer A

机构信息

Unité de Recherches sur la Régulation de la Croissance, Institut National de la Santé et de la Recherche Médicale U.142, Hôpital Saint-Antoine, Paris, France.

出版信息

Biochem Biophys Res Commun. 1993 Oct 15;196(1):480-6. doi: 10.1006/bbrc.1993.2275.

DOI:10.1006/bbrc.1993.2275
PMID:7692852
Abstract

In the liver, expression of insulin-like growth factor binding protein-1 (IGFBP-1) is regulated essentially at the transcriptional level, at least in part by HNF1. In this study, the functional role of DBP and C/EBP (which have several potential binding sites on the IGFBP-1 proximal promoter) have been investigated. Transient co-transfection of the reporter plasmid, pBP-1341 and eukaryotic expression vectors which code for DBP and C/EBP in human cell lines Hep3B, HepG2 and C33 showed that IGFBP-1 promoter activity was unchanged by C/EBP, but increased between 2 and 7 times by DBP (depending on the cell line). In addition, DBP and HNF1 were capable of functional co-operation in activating the IGFBP-1 promoter. Our results support the notion of DBP being involved in limited tissue specificity of IGFBP-1 expression.

摘要

在肝脏中,胰岛素样生长因子结合蛋白-1(IGFBP-1)的表达主要在转录水平受到调控,至少部分是由肝细胞核因子1(HNF1)调控。在本研究中,已对DBP和C/EBP(它们在IGFBP-1近端启动子上有几个潜在结合位点)的功能作用进行了研究。在人细胞系Hep3B、HepG2和C33中,将报告质粒pBP-1341与编码DBP和C/EBP的真核表达载体进行瞬时共转染,结果显示,C/EBP对IGFBP-1启动子活性无影响,但DBP可使其活性增加2至7倍(取决于细胞系)。此外,DBP和HNF1在激活IGFBP-1启动子方面具有功能协同作用。我们的结果支持DBP参与IGFBP-1表达的有限组织特异性这一观点。

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Interplay of the liver-enriched trans-acting factors, DBP and HNF1, in the transactivation of human IGFBP-1 promoter.肝脏富集反式作用因子DBP和HNF1在人胰岛素样生长因子结合蛋白-1(IGFBP-1)启动子反式激活中的相互作用
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引用本文的文献

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Interleukin-6-induced STAT3 and AP-1 amplify hepatocyte nuclear factor 1-mediated transactivation of hepatic genes, an adaptive response to liver injury.白细胞介素-6诱导的信号转导和转录激活因子3(STAT3)及活化蛋白-1(AP-1)增强肝细胞核因子1介导的肝脏基因反式激活,这是对肝损伤的一种适应性反应。
Mol Cell Biol. 2001 Jan;21(2):414-24. doi: 10.1128/MCB.21.2.414-424.2001.