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Papers In Press, published online ahead of print February 22, 2001
MRC clinical sciences centre, Imperial College School of Medicine, London W12 ONN
Corresponding Author: a.sardini{at}csc.mrc.ac.uk
Volume regulation is essential for normal cell function. A key component of the cells' response to volume changes is the activation of a channel which elicits characteristic chloride currents (ICl,Swell). The molecular identity of this channel has been controversial. Most recently ClC-3, a protein highly homologous to the ClC-4 and ClC-5 channel proteins, has been proposed as responsible for ICl,Swell (1). Subsequently, however, other reports have suggested that ClC-3 may generate chloride currents with characteristics clearly distinct from ICl,Swell. Significantly different tissues distributions for ClC-3 have also been reported and it has been suggested that two isoforms of ClC-3 may be expressed with differing functions. In this study we generated a series of cell lines expressing variants of ClC-3 to rigorously address the question of whether or not ClC-3 is responsible for ICl,Swell. The data demonstrate that ClC-3 is not responsible for ICl,Swell and has no role in RVD, furthermore, ClC-3 is not activated by intracellular calcium and fails to elicit chloride currents under any conditions tested. Expression of ClC-3 was shown to be relatively tissue specific, with high levels in the central nervous system and kidney, and in contrast to previous reports, is essentially absent from heart. This distribution is also inconsistent with the previous proposed role in cell volume regulation.
J. Biol. Chem, 10.1074/jbc.M011667200
Submitted on December 26, 2000
Revised on February 22, 2001
Accepted on February 22, 2001
Human ClC-3 is not the swelling-activated chloride channel involved in cell volume regulation
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