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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2013 Jul;62(1):22–25. doi: 10.1097/FJC.0b013e31829709d4

Figure 1.

Figure 1

Agonists and antagonists of membrane-associated subpopulations (mER) of ERα and ERβ, as opposed to GPER with intrinsic activity mediating or inhibiting rapid estrogen signaling. Green arrows: activation, red arrows: inhibition, and the orange arrow: tissue-dependent activation or inhibition. Effects can be achieved by natural (endogenous estrogen such as 17β-estradiol) as well as by synthetic drugs (selective agonists for ERα, ERβ, or GPER), SERMS, SERDs, plant-derived substances (genistein), or highly stable environmental pollutants and xenoestrogens (atrazine, zearalonone, bisphenol A, nonylphenol, or DDT). SERM, selective estrogen receptor modulator; SERD, selective estrogen receptor downregulator. Figure modified from Steroids 2012; 77:935-942. M. Barton: Position paper: The membrane estrogen receptor GPER--Clues and questions, with permission of Elsevier Publishers.