GPER

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GPER

A gene on chromosome 7p22.3 that encodes a G protein-coupled receptor that binds oestrogen and is widely distributed in neural, breast cancer, placental, heart, ovarian, prostate, hepatic, vascular epithelial and lymphoid tissue. It plays a role in rapid nongenomic signalling events seen after oestrogen stimulation of cells and tissues.
References in periodicals archive ?
Binding and activation of the seven-transmembrane estrogen receptor GPR30 by environmental estrogens: A potential novel mechanism of endocrine disruption.
Lead investigator Shuk-mei Ho, PhD, chairwoman of the Department of Environmental Health at the University of Cincinnati and her team previously found they can inhibit the growth of prostate cancer cell lines in culture by targeting and activating a protein called G protein-coupled receptor 30 (GPR30) using the experimental drug G-1, a GPR30 agonist, or stimulator.
2]-stimulation also occurs via different mechanisms like GPR30 receptors (Kamanga-Sollo et al.
Hung-Ming Lam has shown that the chemical compound G1 tightly binds GPR30 in highly selective manner and this G1-GPR30 complex inhibits the growth of prostate cancer cells.
G protein-coupled receptor 30 (GPR30) mediates gene expression changes and growth response to 173-estradiol and selective GPR30 ligand G-1 in ovarian cancer cells.
The G protein-coupled receptor GPR30 mediates c-fos up-regulation by 17beta-estradiol and phytoestrogens in breast cancer cells.
2008; Jeng and Watson 2011), although, as in our past studies, ER[beta] and GPR30 also contributed to this ERK response to estrogens.
Membranes were probed overnight at 4[degrees]C with antibodies against c-Fos (H-125), [beta]-actin (C-2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2; E-4), Egr-1 (588), CTGF (L-20), ERK2 (C-14), ER[alpha] (F-10), or GPR30 (N-15), all from Santa Cruz Biotechnology, DBA (Milan, Italy), or ER[beta] from Serotec (Space Import Export, Milan, Italy).
heart, muscle, brain); this may indicate that estrogen signaling requires tissue-specific cofactors or coreceptors to activate the estrogen cascade and/or that signaling operates through the membrane-associated ER GPR30 (G proteincoupled receptor 30) in some tissues (Filardo a al.
The authors report that BPA activated the PKG and EGFR/ERK/c-fos pathways through cross-talk between GPR30 and ER-[alpha], which in turn stimulated GC-1 cell proliferation.
CONCLUSIONS: Our data suggest that low concentrations of BPA activate the PKG and EGFR/ERK/ c-foes pathways through a cross-talk between GPR30 and ER-[alpha], which in turn stimulates GC-1 cell proliferation.