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. 2018 Nov 27;9:708. doi: 10.3389/fendo.2018.00708

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Copyright © 2018 Krick, Helton, Hutcheson, Blumhof, Garth, Denson, Zaharias, Wickham and Barnes.

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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The NFAT activation is regulated by FGF23 and OGA inhibition (TG) and is downstream of O-GlcNAc regulation. (A) FGF23 and TG activate NFAT as assessed by a luciferase-based reporter gene assay in HBECs and is reduced to normal levels by an FGFR4 inhibitor (R4) or blocked by OSMI-1 similar to the effects of the NFAT activation inhibitor, cyclosporine (CsA). (B) Western blots of O-GlcNAc, OGT, and OGA following knockdown of NFAT2c and NFAT3c. Experiments were performed in triplicate. Statistical analysis was done using ANOVA or Student's t-test showing means ± S.E.M. with ^*p < 0.05, and ^***p < 0.001. Ctrl, Control; FGF23, fibroblast growth factor 23; TG, thiamet G (OGA inhibitor); R4, FGFR4 inhibitor; OSMI-1, OGT inhibitor; CsA, cyclosporine; and siNFAT, small interfering RNA against NFAT2c or 3c.