Advances in the understanding of the structure and function of ER-α36,a novel variant of human estrogen receptor-alpha

被引：33

作者：

Rao, Jun ^{[1
]}

Jiang, Xiaomei ^{[1
]}

Wang, Yang ^{[1
]}

Chen, Bin ^{[1
]}

机构：

[1] Third Mil Med Univ, Dept Biochem & Mol Biol, Chongqing 400038, Peoples R China

来源：

JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY | 2011年 / 127卷 / 3-5期

基金：

中国国家自然科学基金;

关键词：

Estrogen receptor; ER-alpha; 36; ER genomic/nongenomic actions; Breast cancer; Endocrine therapy resistance; RETRACTED ARTICLE. SEE; BREAST-CANCER; ER-ALPHA; NONGENOMIC ACTIONS; ENDOCRINE THERAPY; PLASMA-MEMBRANE; AROMATASE INHIBITORS; POSTMENOPAUSAL WOMEN; GENE-EXPRESSION; MESSENGER-RNAS;

D O I：

10.1016/j.jsbmb.2011.08.004

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：

Estrogen receptors (ERs) belong to the nuclear receptor superfamily, whose members include ER-alpha 66, ER-alpha 36, ER-alpha 46 and ER-beta. Each receptor performs specific functions through binding with a specific ligand, such as estrogen. Recently, ER-alpha 36, a novel variant of human estrogen receptor-alpha (ER-alpha), was identified and cloned. ER-alpha 36 inhibits, in a dominant-negative manner, the transactivation of both the wild-type ER-alpha (ER-0.66) and ER-P. As a predominantly membrane-based ER, ER-alpha 36 mediates nongenomic estrogen signaling and is involved in the resistance of breast cancer to endocrine therapy, i.e., tamoxifen. This review summarizes recent studies on the structure and function of ER-alpha 36 and the relationship of ER-alpha 36 with cancer, with special emphasis on its function in the resistance of breast cancer to endocrine therapy. (C) 2011 Elsevier Ltd. All rights reserved.

引用

页码：231 / 237

页数：7

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