ClC-2 Channels in Erythrocytes



Ekaterina Shumilina1, Stephan M. Huber*, 2
1 Department of Physiology, University of Tübingen, Germany
2 Department of Radiation Oncology, University of Tübingen, Germany


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© 2011 Shumilina and Huber

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Radiation Oncology, University of Tübingen, Hoppe-Seyler-Str. 3, 72076 Tübingen, Germany; Tel: +49-(0)7071-29-82183; Fax: +49-(0)7071-29-4944; E-mail: stephan.huber@uni-tuebingen.de


Abstract

ClC-2 is a ubiquitously expressed plasma membrane Cl- channel that reportedly controls the ionic environment in mouse retina and testis. Beyond that, ClC-2 might sense cellular energy status and cellular stress by its carboxyterminal cystathionine-beta-synthase (CBS) domains and by its molecular interaction with the heat shock protein Hsp90, respectively. In mature human and mouse erythrocytes, ClC-2 is activated by oxidative stress and by malaria infection. This article describes possible function of erythrocyte ClC-2 channels for the programmed death of oxidatively injured erythrocytes and for the regulatory volume decrease of malaria-infected erythrocytes.

Keywords: Patch-clamp whole cell recording, red blood cell, chloride channel, oxidative stress, cystathionine-beta-synthase domain.