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. 2021 Jul 20;66(9):927–935. doi: 10.1038/s10038-021-00962-6

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Pathophysiological role of the BIG3-PHB2 complex in estrogen-dependent breast cancer cells. Estrogen (E2) stimulation induces PKA-dependent BIG3 phosphorylation, which cancels its negative regulation of PP1Cα activity, resulting in the avoidance of PHB2 suppressive activity (Upper panel). stERAP competitively binds to endogenous PHB2, thereby preventing its interactions with BIG3. Free PHB2 directly binds to both nuclear and plasma membrane-associated ERα, resulting in repression of E2-induced genomic and non-genomic ERα activation (Lower panel)