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. 2020 Oct 21;8:556543. doi: 10.3389/fcell.2020.556543

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Copyright © 2020 Lang, Rajaxavier, Singh, Brucker and Salker.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SGK1 in infertility: A transient decline of SGK1 activity in the endometrial epithelium promotes blastocyst apposition by regulating the activities of Epithelial sodium channel (ENaC) and Cystic fibrosis transmembrane conductance regulator (CFTR) to achieve appropriate uterine luminal fluid (ULF) secretion and absorption during the window of endometrial receptivity to confer successful implantation. Whereas, when expressed in high levels in the luminal epithelium, SGK1 is speculated to perturb uterine luminal fluid balance, attenuate endometrial receptivity and thereby resulting in implantation failure.