The Open Biology Journal
2011, 04 : 18-26Published online 2011 January 31. DOI: 10.2174/1874196701104010018
Publisher ID: TOBIOJ-4-18
RESEARCH ARTICLE
ClC-2 Channels in Erythrocytes
1
Department of Physiology, University of Tübingen, Germany
2 Department of Radiation Oncology, University of Tübingen, Germany
* 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
2 Department of Radiation Oncology, University of Tübingen, Germany
* 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.