Estrogen-induced activation of Erk-1 and Erk-2 requires the G protein-coupled receptor homolog, GPR30, and occurs via trans-activation of the epidermal growth factor receptor through release of…

By E. Filardo, Jeffrey A. Quinn, K. Bland, A. Frackelton, Roger Williams. Molecular Endocrinology, 2000

1,394 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Oncology

View Paper: https://www.semanticscholar.org/paper/da800350cb244bcb819e91671962270436d462ed

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In Cancer Research

1. P. Thomas
2. E. Levin

In Genetics

1. Vera Regitz-Zagrosek
2. P. Thomas
3. Georgios Kararigas

In Oncology

1. Tudor I. Oprea
2. E. Levin
3. Marcello Maggiolini
4. Rosamaria Lappano

Citations in the corpus

• Virtual and biomolecular screening converge on a selective agonist for GPR30 (2006, background): “The specificity of the response is shown by the fact that neither 17b-estradiol nor G-1 has an effect on control COS7 cells (not expressing GPR30) and that 17a-estradiol (6) has no effect on GPR30-expressing COS7 cells.”
• Identification of a Structural Determinant Necessary for the Localization and Function of Estrogen Receptor α at the Plasma Membrane (2003, background): “These include G proteins, nonreceptor and receptor tyrosine kinases (Src, EGFR), and threonine-serine kinases, such as phospha* Corresponding author.”
• G protein-coupled receptors: novel targets for drug discovery in cancer (2010, background): “Agonist stimulation of diverse GPCRs, such as thrombin, LPA, oestrogen, bombesin and endothelin, can lead to transactivation of epidermal growth factor (EGF) receptor (EGFR) through autocrine and paracrine release of EGF-like ligands tethered at the cell surface and the subsequent generation of in”
• Identity of an estrogen membrane receptor coupled to a G protein in human breast cancer cells. (2005, methodology): “Estrogens can activate pathways involved in proliferative responses, such as MAPK via EGFR transactivation and c-fos expression, in nER-negative breast cancer cells via GPR30 (24, 38).”
• Mechanistic Pathways of Sex Differences in Cardiovascular Disease. (2017, background): “A third receptor, the G protein-coupled receptor (GPR30), has been proposed to be an ER mediating nongenomic effects of E2 (117, 118, 335), whose role, though, as an actual ER binding E2 in a direct manner or an interacting partner of the classical ER has been debated (221, 297).”