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María Andrea Camilletti, Alejandra Abeledo-Machado, Jimena Ferraris, Pablo A Pérez, Erika Y Faraoni, Daniel Pisera, Silvina Gutierrez and Graciela Díaz-Torga

membrane ( Zhang et al. 2011 , 2012 , Zarate et al. 2012 , Micevych et al. 2017 ), the involvement of the 7-transmembrane G protein-coupled estrogen receptor (GPER, formerly named GPR30) in estradiol-induced rapid, non-genomic events has been in

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Joseph Aizen and Peter Thomas

-coupled estrogen receptor 1 (GPER1), formerly known as GPR30, is a novel, specific seven-transmembrane-domain estrogen receptor coupled to a stimulatory G protein (G s ) that mediates rapid, nongenomic estrogen actions through activation of adenylyl cyclase and

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Kimberley D Katleba, Erin L Legacki, Alan J Conley and Trish Berger

125 μg fulvestrant, a nuclear estrogen receptor (ESR1 and ESR2) antagonist and G protein-coupled estrogen receptor (GPER) agonist (Tocris USA, Ellisville, MO, USA)/kg body weight per day via Alzet osmotic pumps (models 2ML4 and 2ML2; Durect Corporation

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Matthias R Meyer, Natalie C Fredette, Matthias Barton and Eric R Prossnitz

including estrogen receptor α ( Green et al . 1986 , Greene et al . 1986 ) and estrogen receptor β ( Kuiper et al . 1996 ), as well as the 7-transmembrane, intracellular G protein-coupled estrogen receptor (GPER) ( Revankar et al . 2005 , Thomas et al

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Stefanie Ruhs, Alexander Nolze, Ralf Hübschmann and Claudia Grossmann

may elicit nongenomic effects by interacting with receptors, i.e. receptor tyrosine kinases like EGFR, PDGFR and IGF1R or GPCR like AT1 or GPER1. Striatin Striatin is a scaffolding protein that contains several protein-binding domains

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Marcello Maggiolini and Didier Picard

official name: G-protein coupled ER1 (GPER). Signal transduction pathways Some of the very first reports already established that the GPCR GPR30 does indeed couple to G-proteins in breast cancer cells. Inhibitor studies and measurements of GTP recruitment

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Matti Poutanen

types. Several studies indicate that rapid estrogen signaling is not mediated via the nuclear ERs, but through the G-protein-coupled ER1 ( GPER , also known as GPR30 ). GPER activates epidermal growth factor receptor (EGFR) by inducing a release of

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Takuya Yoshino, Tomohisa Nagoshi, Ryuko Anzawa, Yusuke Kashiwagi, Keiichi Ito, Daisuke Katoh, Masami Fujisaki, Yosuke Kayama, Taro Date, Kenichi Hongo and Michihiro Yoshimura

glucocorticoid receptor (GR)/progesterone receptor antagonist RU486 (Sigma–Aldrich), 10 −7  mol/l of the G protein-coupled estrogen receptor (GPER, previously known as G protein-coupled receptor 30 (GPR30)) antagonist G15 (Cayman Chemical, Ann Arbor, MI, USA), or

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Claire V Hutchinson, James A Walker and Colin Davidson

. Recently, a G protein-coupled oestrogen receptor (GPER – previously known as GPR30) has been identified, which acts at the cell surface and is found in a variety of tissues ( Hazell et al . 2009 , Filardo & Thomas 2012 ). Whereas the nuclear receptors

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Joseph Aizen, Lian Hollander-Cohen, Michal Shpilman and Berta Levavi-Sivan

shift, E2 and its 7TMD receptors (GPR30 = GPER) in the oocytes maintain meiotic arrest. Therefore, the decrease in E2 is essential for the resumption of meiosis during oocyte maturation ( Pang & Thomas 2009 , Pang & Thomas 2010 ). Recent work by