Publication Name	World Journal of Nephrology
Manuscript ID	29408
Country	Japan

Received	2016-08-12 08:55
Peer-Review Started	2016-08-12 14:09
To Make the First Decision	2016-09-30 11:23
Return for Revision	2016-09-30 14:37
Revised	2016-10-04 15:01
Second Decision	2016-10-28 11:27
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2016-11-02 16:18
Articles in Press	2016-11-02 16:18
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2016-12-26 13:13
Publish the Manuscript Online	2016-12-28 15:40

ISSN	2220-6124 (online)
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/
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Category	Urology & Nephrology
Manuscript Type	Minireviews
Article Title	Functional coupling of V-ATPase and CLC-5
Manuscript Source	Invited Manuscript
All Author List	Nobuhiko Satoh, Masashi Suzuki, Motonobu Nakamura, Atsushi Suzuki, Shoko Horita, George Seki and Kyoji Moriya
Funding Agency and Grant Number
Corresponding Author	Nobuhiko Satoh, MD, Department of Internal Medicine, Faculty of Medicine, the University of Tokyo Hospital, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. nosatou-tky@umin.ac.jp
Key Words	V-ATPase; CLC-5; Endocytosis; Endosomal acidification; Dent’s disease; Gating glutamate; E211Q
Core Tip	Chloride channel 5 (CLC-5) mutations cause Dent’s disease, which is characterized by renal proximal tubulopathy due to defective endocytosis. Recent revelations that CLC-5 is a 2Cl-/H+ antiporter and not a Cl- channel challenged the classical model proposing CLC-5 as a Cl- shunt to facilitate V-ATPase-mediated endosomal acidification. Therefore, physiological roles of CLC-5 and its interaction with V-ATPase in endosomal acidification and/or endocytosis are intensely debated. Recent functional analysis of a novel pure Cl- channel mutant from a Dent’s disease patient indicated a possible functional coupling between V-ATPase and CLC-5 not only in endosomal acidification but also at the plasma membrane.
Publish Date	2016-12-28 15:40
Citation	Satoh N, Suzuki M, Nakamura M, Suzuki A, Horita S, Seki G, Moriya K. Functional coupling of V-ATPase and CLC-5. World J Nephrol 2017; 6(1): 14-20
URL	http://www.wjgnet.com/2220-6124/full/v6/i1/14.htm
DOI	http://dx.doi.org/10.5527/wjn.v6.i1.14

Full Article (PDF)	WJN-6-14.pdf
Full Article (Word)	WJN-6-14.doc
Manuscript File	29408-Review.docx
Answering Reviewers	29408-Answering reviewers.pdf
Audio Core Tip	29408-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	29408-Conflict-of-interest statement.pdf
Copyright License Agreement	29408-Copyright assignment.pdf
Non-Native Speakers of English Editing Certificate	29408-Language certificate.pdf
Peer-review Report	29408-Peer-review(s).pdf
Scientific Misconduct Check	29408-Scientific misconduct check.pdf
Scientific Editor Work List	29408-Scientific editor work list.pdf