Estrogen receptor-alpha (ER-α) suppresses expression of its variant ER-α36

被引：83

作者：

Zou, Yi ^{[1
]}

Ding, Ling ^{[1
]}

Coleman, Megan ^{[1
]}

Wang, Zhaoyi ^{[1
]}

机构：

[1] Creighton Univ, Sch Med, Dept Med Microbiol & Immunol, Omaha, NE 68178 USA

来源：

FEBS LETTERS | 2009年 / 583卷 / 08期

关键词：

Promoter; Estrogen receptor; ER-alpha; 36; Breast cancer; HUMAN BREAST CARCINOMAS; ELEMENT HALF-SITE; BINDING-SITES; IDENTIFICATION; GROWTH; GENE; ACTIVATION; PATHWAYS; CANCER; WT1;

D O I：

10.1016/j.febslet.2009.03.047

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：

Recently, we identified and cloned a membrane-based estrogen receptor (ER), ER-alpha 36, which is transcribed from a previously unidentified promoter in the first intron of the original ER-alpha gene. We cloned the 5' flanking region of ER-alpha 36 and found the cloned DNA sequence possessed strong promoter activity. A single transcription initiation site was mapped and a number of putative regulatory elements for various transcription factors such as the Wilms' tumor suppressor, WT1 and estrogen receptor (ER) were identified in this region. Transient co-transfection experiments further demonstrated that ER-alpha suppresses ER-alpha 36 promoter activity in an estrogen-independent manner, which can be released by ER-alpha 36 itself. (C) 2009 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.

引用

页码：1368 / 1374

页数：7

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