Trichostatin A activates the osteopontin gene promoter through AP1 site

被引：37

作者：

Sakata, R ^{[1
]}

Minami, S

Sowa, Y

Yoshida, M

Tamaki, T

机构：

[1] Wakayma Med Univ, Dept Orthoped Surg, Wakayama 6418510, Japan

[2] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Mol Targeting Canc Prevent, Kamigyo Ku, Kyoto 6028566, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 315卷 / 04期

关键词：

trichostatin A; osteopontin; AP1; HDAC inhibitor; promoter assay;

D O I：

10.1016/j.bbrc.2004.01.152

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In this study, we investigated osteoblastic differentiation by trichostatin A (TSA), a historic deacetylase inhibitor in mouse undifferentiated mesenchymal cell line. TSA increased the osteopontin (OPN) mRNA level and OPN protein. Deletion analysis of the promoter region revealed TSA-induced luciferase response was regulated by -75 to -65 of the OPN promoter. There was an AP1-binding sequence at the site of the OPN promoter. In an electrophoretic mobility shift assay, bands of the complexes were supershifted by addition of antibody to c-fos and phosphorylated c-jun. These data suggested that AP1 plays a crucial role in the TSA-induced OPN expression. (C) 2004 Elsevier Inc. All-rights reserved.

引用

页码：959 / 963

页数：5

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