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. 2014 Aug 30;7:1525–1533. doi: 10.2147/OTT.S65345

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© 2014 Su et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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Genomic and non-genomic activities mediated by ERs.

Notes: ER-α66 binds to estrogen and then transfers to the nucleus to interact with specific EREs and induce transcription of target genes. ER-α36 has a broader ligand-binding spectrum than ER-α66 so that it can respond to E2α, E2β, E3, E4, and even tamoxifen. ER-α36 can mediate rapid MIES such as MAPK/ERK, PI3K/Akt, and PKC δ to regulate biological functions of cells.

Abbreviations: Akt, protein kinase B; BCSCs, breast cancer stem cells; cdk 4, cyclin-dependent kinase 4; ER-α36, estrogen receptor-alpha36; ER-α66, estrogen receptor-alpha66; EREs, estrogen response elements; ERK, extracellular signal-regulated kinase; ERs, estrogen receptors; GSK3 β, glycogen synthase kinase 3 beta; JNKs, c-Jun N-terminal kinases; MAPK, mitogen-activated protein kinases; MIES, membrane-initiated estrogen signaling; PKC δ, protein kinase C delta; PI3K, phosphatidylinositide 3-kinase.