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人上皮细胞中髓样 Elf-1 样因子的 Sp1 依赖性调控

Sp1-dependent regulation of Myeloid Elf-1 like factor in human epithelial cells.

作者信息

Koga Tomoaki, Suico Mary Ann, Nakamura Hideaki, Taura Manabu, Lu Zhuo, Shuto Tsuyoshi, Okiyoneda Tsukasa, Kai Hirofumi

机构信息

Department of Molecular Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Japan.

出版信息

FEBS Lett. 2005 May 23;579(13):2811-6. doi: 10.1016/j.febslet.2005.04.015. Epub 2005 Apr 21.

Abstract

Myeloid Elf-1 like factor (MEF) is an ETS protein, which activates the promoters of granulocyte macrophage colony-stimulating factor, interleukin-3, lysozyme, human beta defensin-2 and perforin. In spite of its many known functions, little is known about MEF transcriptional regulation. Here, we cloned the 5'-flanking region of human MEF gene and identified a TATA-less promoter region at -204/-54 which contains 4 putative binding sites for Sp1, two of which are essential in up-regulating MEF activity. These were proven by EMSA and blocking Sp1 using RNAi or mithramycin A treatment of HEK293 cells. Our results suggest that Sp1 constitutively regulates the MEF gene.

摘要

髓样 Elf-1 样因子(MEF)是一种 ETS 蛋白,它可激活粒细胞巨噬细胞集落刺激因子、白细胞介素-3、溶菌酶、人β-防御素-2 和穿孔素的启动子。尽管已知其多种功能,但对 MEF 的转录调控了解甚少。在此,我们克隆了人 MEF 基因的 5'侧翼区域,并在-204/-54 处鉴定出一个无 TATA 框的启动子区域,该区域包含 4 个假定的 Sp1 结合位点,其中两个对于上调 MEF 活性至关重要。通过电泳迁移率变动分析(EMSA)以及对 HEK293 细胞使用 RNAi 或光神霉素 A 处理来阻断 Sp1 证实了这一点。我们的结果表明 Sp1 组成性地调节 MEF 基因。

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