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 ?
Virtual and biomolecular screening converge on a selective agonist for GPR30. Nat Chem Biol 2(4):207-212, PMID: 16520733, https://doi.org/10.1038/ nchembio775.
G protein-coupled receptor 30 (GPR30) acts as plasma membrane receptor and shows biological activities of estrogen [12,13].
Zhou et al., "Imbalance between proliferation and apoptosis-related impaired GPR30 expression is involved in preeclampsia," Cell and Tissue Research, vol.
In addition to nuclear receptors, there is a third ER, namely GPR30, which belongs to the G protein-coupled receptor family.
Vasudevan, "GPR30 activation decreases anxiety in the open field test but not in the elevated plus maze test in female mice," Brain and Behavior, vol.
GPER is a membrane estrogen receptor, a 7-transmembrane spanning G-protein-coupled receptor, also called G-protein-coupled receptor 30 (GPR30) [13].
There are two types of ERs: one type is nuclear estrogen receptors (nERs), which are members of the nuclear receptor family of intracellular receptors, including ERa and ER; the other type is membrane estrogen receptors (mERs), which are mostly G protein-coupled receptors, including Gq-coupled mER (Gq-ER), GPER1 (formerly GPR30), and ER-X [27].
As a family of G proteins, estrogen-associated G protein-coupled receptor 30 (GPR30) was detected in many human tissues, including ovary and prostate (Prossnitz et al., 2008).
Rapid non-genomic responses to estrogen are mediated by either ERs at the plasma membrane [5] or the extranuclear seven-transmembrane domain receptor (GPR30) [6].
Other study also reported the inhibition of TGF-[beta] signaling by E2, in which mitogen-activated protein kinases (MAPKs) activated by E2 via G protein-coupled receptor 30 (GPR30) inhibited the activation of Smad proteins, downstream molecules of TGF-[beta] signaling (Kleuser et al.
Liu et al., "The interactions between GPR30 and the major biomarkers in infiltrating ductal carcinoma of the breast in an Asian population," Taiwanese Journal of Obstetrics and Gynecology, vol.
GPR30, but not estrogen receptor-alpha, is crucial in the treatment of experimental autoimmune encephalomyelitis by oral ehinyl estradiol.