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学科主题: 药学
题名:
Involvement of Estrogen Receptor Variant ER-alpha 36, Not GPR30, in Nongenomic Estrogen Signaling
作者: Kang, Lianguo1; Zhang, Xintian1; Xie, Yan2; Tu, Yaping2; Wang, Dong3; Liu, Zhenming3; Wang, Zhao-Yi1
刊名: MOLECULAR ENDOCRINOLOGY
发表日期: 2010-04-01
DOI: 10.1210/me.2009-0317
卷: 24, 期:4, 页:709-721
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism
研究领域[WOS]: Endocrinology & Metabolism
关键词[WOS]: BREAST-CANCER CELLS ; PROTEIN-COUPLED RECEPTOR-30 ; ER-ALPHA ; G-PROTEIN-COUPLED-RECEPTOR-30 GPR30 ; PLASMA-MEMBRANE ; RAPID ACTION ; ESTRADIOL HYPERSENSITIVITY ; EXPRESSION ; ACTIVATION ; KINASE
英文摘要:

Accumulating evidence suggested that an orphan G protein-coupled receptor (GPR)30, mediates nongenomic responses to estrogen. The present study was performed to investigate the molecular mechanisms underlying GPR30 function. We found that knockdown of GPR30 expression in breast cancer SK-BR-3 cells down-regulated the expression levels of estrogen receptor (ER)-alpha 36, a variant of ER-alpha. Introduction of a GPR30 expression vector into GPR30 nonexpressing cells induced endogenous ER-alpha 36 expression, and cotransfection assay demonstrated that GPR30 activated the promoter activity of ER-alpha 36 via an activator protein 1 binding site. Both 17 beta-estradiol (E2) and G1, a compound reported to be a selective GPR30 agonist, increased the phosphorylation levels of the MAPK/ERK1/2 in SK-BR-3 cells, which could be blocked by an anti-ER-alpha 36-specific antibody against its ligand-binding domain. G1 induced activities mediated by ER-alpha 36, such as transcription activation activity of a VP16-ER-alpha 36 fusion protein and activation of the MAPK/ERK1/2 in ER-alpha 36 expressing cells. ER-alpha 36-expressing cells, but not the nonexpressing cells, displayed high-affinity, specific E2 and G1 binding, and E2- and G1-induced intracellular Ca2+ mobilization only in ER-alpha 36 expressing cells. Taken together, our results demonstrated that previously reported activities of GPR30 in response to estrogen were through its ability to induce ER-alpha 36 expression. The selective G protein-coupled receptor (GPR) 30 agonist G1 actually interacts with ER-alpha 36. Thus, the ER-alpha variant ER-alpha 36, not GPR30, is involved in nongenomic estrogen signaling. (Molecular Endocrinology 24: 709-721, 2010)

语种: 英语
所属项目编号: DK070016 ; LB-595 ; LB692
项目资助者: National Institutes of Health ; Nebraska Tobacco Settlement Biomedical Research Program
WOS记录号: WOS:000276051300003
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59055
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Creighton Univ, Sch Med, Dept Pharmacol, Omaha, NE 68178 USA
2.Creighton Univ, Sch Med, Dept Immunol & Med Microbiol, Omaha, NE 68178 USA
3.Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100083, Peoples R China

Recommended Citation:
Kang, Lianguo,Zhang, Xintian,Xie, Yan,et al. Involvement of Estrogen Receptor Variant ER-alpha 36, Not GPR30, in Nongenomic Estrogen Signaling[J]. MOLECULAR ENDOCRINOLOGY,2010,24(4):709-721.
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