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G protein-coupled estrogen receptor (GPER), or GPR30, specifically binds natural and man-made estrogens.[1] It is thought to be involved in estrogen-sensitive cancers.[1],[2] GPER knockout mice are fertile, although they exhibit thymic atrophy, impaired glucose tolerance, and altered bone growth.[1] G-36 is a cell-permeable non-steroidal antagonist of GPER, inhibiting activation by either 17β-estradiol or the GPER-selective agonist G-1 (IC50 = 112 and 165 nM, respectively).[3] It has no detectable binding activity to either ERα or ERβ.3 G-36 blocks the activation of PI3K or calcium mobilization triggered by estrogen through GPER and it suppresses ERK activation by estrogen or G-1 but not by EGF.[3] G-36 can be used in combination with GPER-selective agonists, like G-1, to distinguish the roles of GPER from those of ERα and ERβ in complex biological systems.[3],[4]

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