Review
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Jan 6, 2016; 5(1): 20-32
Published online Jan 6, 2016. doi: 10.5527/wjn.v5.i1.20
How do kinases contribute to tonicity-dependent regulation of the transcription factor NFAT5?
Xiaoming Zhou
Xiaoming Zhou, Division of Nephrology, Department of Medicine, Uniformed Services University, Bethesda, MD 20814, United States
Author contributions: Zhou X drafted, edited and approved the manuscript.
Conflict-of-interest statement: The author declares no conflict-of-interest for this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Xiaoming Zhou, PhD, Division of Nephrology, Department of Medicine, Uniformed Services University, 4301 Jones Bridge Road, Bethesda, MD 20814, United States. xiaoming.zhou@usuhs.edu
Telephone: +1-301-2959604 Fax: +1-301-2953557
Received: September 5, 2015
Peer-review started: September 8, 2015
First decision: September 29, 2015
Revised: October 19, 2015
Accepted: December 9, 2015
Article in press: December 11, 2015
Published online: January 6, 2016
Processing time: 123 Days and 22.7 Hours
Core Tip

Core tip: NFAT5 is critical for kidney functions. Its dis-regulation results in or is associated with the renal diseases and disorders. More than a dozen of kinases have been identified to contribute to tonicity-dependent regulation of NFAT5. The present review is focused on how these kinases regulate NFAT5 activity under the context of hypertonicity or hypotonicity. Understanding these regulatory mechanisms will have therapeutic implications. A precedent example is that recognition of the cyclosporine immunosuppressive effect resulted from inhibition of the phosphatase calcineurin-dependent activation of NFAT1 allows combination use of cyclosporine with other mechanistically different immunosuppressants to improve their therapeutic efficacy and reduce their side effects.