Barton, "The G-protein-coupled estrogen receptor
GPER in health and disease," Nature Reviews Endocrinology, vol.
In addition,
GPER is also highly expressed in human macrophages [201].
Because of the lack of specificity of estrogen and anti-estrogens for the three known estrogen receptors (ER[alpha], ER[beta], and
GPER), we have developed both a GPER-selective agonist (G-1, [40]) and antagonists (G15 [41]and G36[42]) that display virtually no activity towards the classical estrogen receptors.
In the present study, we quantified the
GPER binding potencies of 12 PBDEs (with bromination numbers from 1 to 8) and 18 OH-PBDEs (with hydroxyl positions of ortho-, meta- and para-) using a fluorescence competitive binding assay in a human breast cancer cell line (SKBR3).
Primer sequences for
GPER and GAPDH are presented in Table 1.
A growing body of evidence suggests that these effects cannot be explained solely by the classical model of steroid hormone action and that 17[beta]-estradiol can also mediate rapid signaling events via pathways that involve transmembrane ERs, such as G-protein-coupled estrogen receptor termed
GPER (Prossnitz et al.
But, pondering some of the
Gper i b deeper meanings behind the act of sending mundane messages to thousands of people she's never met, she asks, rhetorically: "Do we think we're funnier than we actually are when on twitter?" " Undoubtedly, Geri, you're a comedyy gem - but unintentionally.
Zingg et al., "Estrogen receptor-[alpha] but not-[beta] or
GPER inhibits high glucose-induced human VSMC proliferation: potential role of ROS and ERK," Journal of Clinical Endocrinology and Metabolism, vol.
mention, 17[beta]-estradiol ([E.sub.2]) inhibited cell proliferation through estrogen receptor (ER) P in human testicular seminoma-derived JKT-1 cells and seminoma tumors, whereas bisphenol A (BPA) promoted growth responses through G protein-coupled estrogen receptor (
GPER) and the activation of protein kinase A and protein kinase G transduction pathways, but not through extracellular-signal-regulated kinase (ERK) signaling (Bouskine et al.
mention, 17[beta]-estradiol ([E.sub.2]) inhibited cell proliferation through estrogen receptor (ER) [beta] in human testicular seminoma-derived JKT-1 cells and seminoma tumors, whereas bisphenol A (BPA) promoted growth responses through G protein-coupled estrogen receptor (
GPER) and the activation of protein kinase A and protein kinase G transduction pathways, but not through extracellular-signal-regulated kinase (ERK) signaling (Bouskine et al.
In this regard, our study and others have demonstrated that
GPER is involved in multiple actions triggered by estrogenic compounds, including environmental contaminants, in a variety of cancer cells as well as in cancer-associated fibroblasts (CAFs) (Albanito et al.