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. 2017 Oct 28;3(4):208–217. doi: 10.1007/s40610-017-0072-8

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© The Author(s) 2018, corrected publication June/2018

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, 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.

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Fig. 1 — Activation of SOCE and TRPM4 as feedback mechanism for SOCE. Upon receptor stimulation, IP₃ is produced and binds to the IP₃ receptor. Subsequently, Ca²⁺ is released from intracellular Ca²⁺ stores. The decrease in Ca²⁺ in the ER results in the dissociation of Ca²⁺ from STIM1 proteins, which cluster and recruit and activate Orai1 channels in the plasma membrane that mediate SOCE. The increase in intracellular Ca²⁺ activates TRPM4. The Na⁺ influx via TRPM4 is a negative feedback mechanism for SOCE (please see text for details)