Activation of the Novel Estrogen Receptor G Protein-Coupled Receptor 30 (GPR30) at the Plasma Membrane

G protein-coupled Receptor 30 (GPR30) Forms a Plasma Membrane Complex with Membrane-associated Guanylate Kinases (MAGUKs) and Protein Kinase A-anchoring Protein 5 (AKAP5) That Constitutively Inhibits cAMP Production

“…Second, our results address the specificity and efficacy of receptor agonists reported currently and present new avenues by which this receptor system may be targeted therapeutically. Third, we show that deleting the PDZ motif influences GPR30 subcellular localization, a clear issue of contention with some investigators claiming that GPR30 is localized exclusively in the endoplasmic reticulum (2), whereas others have shown that receptors can clearly be identified in the plasma membrane (13,19,(45)(46)(47). Interestingly, endoplasmic reticulum localization was concluded using a GPR30 construct fused at the C terminus with GFP (2), a modification that has been shown previously to alter trafficking of both GPR30 (46) and GluR1 from this compartment (38) and that we show here FIGURE 9.…”

G-protein-coupled receptors and islet function—Implications for treatment of type 2 diabetes

“…The signaling events caused by estrogen are elevation of cAMP, Ca 2+ release and activation of protein kinases. Recently, the GPCR GPR30 was suggested to be an estrogen receptor (Filardo et al, 2007;Filardo et al, 2000;Kanda & Watanabe, 2003). It has been shown that estrogen protects islets from apoptosis (Le May et al, 2006) and it is therefore possible that GPR30 may be involved in the regulation of islet mass.…”

In Vivo Functions of GPR30/GPER-1, a Membrane Receptor for Estrogen: From Discovery to Functions In Vivo

“…another group has cloned GPR30 as a gene expressed and that GPR30 is present in the plasma membrane [13,14], although a consensus about this has yet to be reached. in general, the data on the localization of GPcR in the endoplasmic reticulum and Golgi apparatus have to be evaluated carefully because the overexpression of exogenous genes often leads to an accumulation in the endoplasmic reticulum due to the use of a strong promoter and the effects of fusion proteins such as GFP.…”