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. 2017 Apr 14;22(4):635. doi: 10.3390/molecules22040635

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hypothetical mechanisms underlying the distinct impact of cardiotonic steroids (CTS) on survival of cells, expressing the CTS-sensitive (α1S) and the CTS-resistant (α1R) Na⁺,K⁺-ATPase subunits. In both cases, saturating levels of CTS strongly increase the [Na⁺]_i/[K⁺]_i ratio. In addition, CTS trigger distinct conformational changes in α1S and α1R isoforms that, in turn, affect their interactions with unknown protein partner(s) I and II. These subsequent signaling events lead to activation of p38 and ERK1/2 MAPK and result in cell death (oncosis) and survival, respectively. “?”, transcriptomic changes and/or other unknown steps of intracellular triggered by elevation of the [Na⁺]_i/[K⁺]_i ratio. Modified from [92].