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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Bone. 2015 Nov;80:67–78. doi: 10.1016/j.bone.2015.04.015

Figure 1.

Figure 1

Molecular mechanisms of action of ERα. a) Classic genomic signalling, in which ligand-activated ERα dimers attach to EREs on DNA and activate or repress transcription. b) ERE-independent genomic signalling, in which ligandactivated ERα binds to other transcription factors (such as the p50 and p65 subunits of NF-κB), which prevent them from binding to their response elements. c,d) Nongenotropic mode of action, in which ligand-activated ERα (in the plasma membrane) activates cytoplasmic kinases which, in turn, induce the phosphorylation of substrate proteins and transcription factors (such as Elk-1 and AP-1) that (c) positively or (d) negatively regulate transcription. Abbreviations: AP-1, transcription factor AP-1; CoA, coenzyme A; Elk-1, ETS domain-containing protein Elk-1; ERα, estrogen receptor α; ERE, estrogen response element; Shc, Shc-transforming protein; SRE, serum response element. Reproduced from: Stavros C. Manolagas, Charles A. O'Brien, and Maria Almeida. Nature Reviews Endocrinology. 2013, 9: 699–712.