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.