An emerging consensus on aquaporin translocation as a regulatory mechanism


Water passes through cell membranes relatively slowly by diffusion. In order to maintain water homeostasis, the rapid and specific regulation of cellular water flow is mediated by the aquaporin (AQP) family of membrane protein water channels. The wide range of tissues that are known to express AQPs is reflected by their involvement in many physiological processes and diseases; thirteen human AQPs have been identified to date and the majority are highly specific for water while others show selectivity for water, glycerol and other small solutes. Receptor mediated translocation, via hormone activation, is an established method of AQP regulation, especially for AQP2. There is now an emerging consensus that the rapid and reversible translocation of other AQPs from intracellular vesicles to the plasma membrane, triggered by a range of stimuli, confers altered membrane permeability thereby acting as a regulatory mechanism. This review examines the molecular components that may enable such AQP regulation; these include cytoskeletal proteins, kinases, calcium and retention or localization signals. Current knowledge on the dynamic regulation of sub-cellular AQP translocation in response to a specific trigger is explored in the context of the regulation of cellular water flow. © 2013 Informa UK, Ltd.

Publication DOI:
Divisions: College of Health & Life Sciences
College of Health & Life Sciences > School of Biosciences > Cellular and Molecular Biomedicine
College of Health & Life Sciences > School of Biosciences
Uncontrolled Keywords: Aquaporin regulation,translocation,water homeostasis,Cell Biology,Molecular Biology
Publication ISSN: 1464-5203
Last Modified: 29 Mar 2024 08:10
Date Deposited: 20 Dec 2012 09:15
Full Text Link: http://informah ... 688.2012.743194
http://www.scop ... tnerID=8YFLogxK
Related URLs: http://www.scop ... tnerID=8YFLogxK (Scopus URL)
PURE Output Type: Article
Published Date: 2013-02
Authors: Conner, Alex C.
Bill, Roslyn M. (ORCID Profile 0000-0003-1331-0852)
Conner, Matthew T.



Version: Accepted Version

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