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Involvement of Estrogen Receptor Variant ER-alpha 36, Not GPR30, in Nongenomic Estrogen Signaling
Kang, Lianguo1; Zhang, Xintian1; Xie, Yan2; Tu, Yaping2; Wang, Dong3; Liu, Zhenming3; Wang, Zhao-Yi1
刊名MOLECULAR ENDOCRINOLOGY
2010-04-01
DOI10.1210/me.2009-0317
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
WOS记录号WOS:000276051300003
项目编号DK070016 ; LB-595 ; LB692
资助机构National Institutes of Health ; Nebraska Tobacco Settlement Biomedical Research Program
引用统计
被引频次:153[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59055
专题北京大学药学院
北京大学药学院_药物化学系
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
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GB/T 7714
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.
APA Kang, Lianguo.,Zhang, Xintian.,Xie, Yan.,Tu, Yaping.,Wang, Dong.,...&Wang, Zhao-Yi.(2010).Involvement of Estrogen Receptor Variant ER-alpha 36, Not GPR30, in Nongenomic Estrogen Signaling.MOLECULAR ENDOCRINOLOGY,24(4),709-721.
MLA Kang, Lianguo,et al."Involvement of Estrogen Receptor Variant ER-alpha 36, Not GPR30, in Nongenomic Estrogen Signaling".MOLECULAR ENDOCRINOLOGY 24.4(2010):709-721.
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