Gating of the voltage-dependent chloride channel CIC-0 by the permeant anion

Nature ◽  
1995 ◽  
Vol 373 (6514) ◽  
pp. 527-531 ◽  
Author(s):  
Michael Pusch ◽  
Uwe Ludewig ◽  
Annett Rehfeldt ◽  
Thomas J. Jentsch
Keyword(s):  
Chloride Channel ◽  
Voltage Dependent ◽  
Permeant Anion

Association between Hsp90 and the ClC-2 chloride channel upregulates channel function

2006 ◽  
Vol 290 (1) ◽  
pp. C45-C56 ◽  
Author(s):  
Alexandre Hinzpeter ◽  
Joanna Lipecka ◽  
Franck Brouillard ◽  
Maryvonne Baudoin-Legros ◽  
Michal Dadlez ◽  
...  
Keyword(s):  
Chloride Channel ◽  
Fluid Transport ◽  
Cell Swelling ◽  
Dependent Manner ◽  
Patch Clamp Technique ◽  
Mass Spectrometry Identification ◽  
Voltage Dependent ◽  
Channel Expression ◽  
Associated Proteins ◽  
Cellular Stresses

The voltage-dependent ClC-2 chloride channel has been implicated in a variety of physiological functions, including fluid transport across specific epithelia. ClC-2 is activated by hyperpolarization, weakly acidic external pH, intracellular Cl−, and cell swelling. To add more insight into the mechanisms involved in ClC-2 regulation, we searched for associated proteins that may influence ClC-2 activity. With the use of immunoprecipitation of ClC-2 from human embryonic kidney-293 cells stably expressing the channel, followed by electrophoretic separation of coimmunoprecipitated proteins and mass spectrometry identification, Hsp70 and Hsp90 were unmasked as possible ClC-2 interacting partners. Association of Hsp90 with ClC-2 was confirmed in mouse brain. Inhibition of Hsp90 by two specific inhibitors, geldanamycin or radicicol, did not affect total amounts of ClC-2 but did reduce plasma membrane channel abundance. Functional experiments using the whole cell configuration of the patch-clamp technique showed that inhibition of Hsp90 reduced ClC-2 current amplitude and impaired the intracellular Cl− concentration [Cl−]-dependent rightward shift of the fractional conductance. Geldanamycin and radicicol increased both the slow and fast activation time constants in a chloride-dependent manner. Heat shock treatment had the opposite effect. These results indicate that association of Hsp90 with ClC-2 results in greater channel activity due to increased cell surface channel expression, facilitation of channel opening, and enhanced channel sensitivity to intracellular [Cl−]. This association may have important pathophysiological consequences, enabling increased ClC-2 activity in response to cellular stresses such as elevated temperature, ischemia, or oxidative reagents.

Attenuation of endothelin effects by a chloride channel inhibitor, indanyloxyacetic acid

1992 ◽  
Vol 262 (5) ◽  
pp. F799-F806 ◽  
Author(s):  
T. Takenaka ◽  
M. Epstein ◽  
H. Forster ◽  
D. W. Landry ◽  
K. Iijima ◽  
...  
Keyword(s):  
Chloride Channel ◽  
Chloride Channels ◽  
Specific Binding ◽  
Fluorescein Isothiocyanate ◽  
Cytosolic Calcium ◽  
Membrane Depolarization ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Afferent Arterioles ◽  
Subsequent Activation

We have recently proposed that the actions of endothelin (ET) are in part mediated by opening of chloride channels (K. Iijima, L. Lin, A. Nasjletti, and M. S. Goligorsky. Am. J. Physiol. 260 (Cell Physiol. 29: C982-C992, 1991). In the present study the ability of a chloride channel inhibitor, an indanyloxyacetic acid (IAA-94), to block ET-induced effects was examined in cultured vascular smooth muscle cells (VSMC) by spectrofluorometry and direct videomicroscopic visualization of the renal microcirculation in isolated perfused hydronephrotic kidneys (IPHK). A fluorescein isothiocyanate (FITC)-labeled IAA-94 analogue showed specific binding to VSMC. IAA-94 (30 microM) neither affected basal cytosolic calcium concentration ([Ca2+]i) in VSMC nor peak response to ET, but it significantly curtailed sustained elevation of [Ca2+]i (half-time recovery was 147 +/- 23 vs. 248 +/- 33 s in control, P less than 0.05). IAA-94 blunted ET-induced membrane depolarization from 24.5 +/- 3.3 to 8.0 +/- 1.8 mV. In IPHK, ET constricted afferent arterioles (AA) by 29 +/- 2% (18.7 +/- 0.8 to 13.2 +/- 0.6 microns, P less than 0.001). Isradipine reversed this ET-induced vasoconstriction. Pretreatment with IAA-94 did not alter AA diameter, but markedly attenuated ET-induced AA constriction (reduction of AA diameters by only 9 +/- 2%, P less than 0.001). The subsequent addition of isradipine (0.1-1 microM) did not further dilate AA. Our data indicate that IAA-94 markedly attenuates AA vasoconstriction elicited by ET and suggest that ET-induced opening of chloride channels, membrane depolarization, and subsequent activation of voltage-dependent calcium channels contribute to the vasoconstrictor mechanisms of this peptide.

scholarly journals Effect of an N‐terminus deletion on voltage‐dependent gating of the ClC‐2 chloride channel

2002 ◽  
Vol 544 (2) ◽  
pp. 363-372 ◽  
Author(s):  
Diego Varela ◽  
María Isabel Niemeyer ◽  
L. Pablo Cid ◽  
Francisco V. Sepúlveda
Keyword(s):  
Chloride Channel ◽  
N Terminus ◽  
Voltage Dependent

scholarly journals Voltage-dependent and -independent titration of specific residues accounts for complex gating of a ClC chloride channel by extracellular protons

2009 ◽  
Vol 587 (7) ◽  
pp. 1387-1400 ◽  
Author(s):  
María Isabel Niemeyer ◽  
L. Pablo Cid ◽  
Yamil R. Yusef ◽  
Rodolfo Briones ◽  
Francisco V. Sepúlveda
Keyword(s):  
Chloride Channel ◽  
Voltage Dependent ◽  
Clc Chloride Channel

scholarly journals Cloning and functional expression of a plant voltage-dependent chloride channel.

1996 ◽  
Vol 8 (4) ◽  
pp. 701-711 ◽  
Author(s):  
C Lurin ◽  
D Geelen ◽  
H Barbier-Brygoo ◽  
J Guern ◽  
C Maurel
Keyword(s):  
Chloride Channel ◽  
Functional Expression ◽  
Voltage Dependent

Two types of chloride channel on duct cells cultured from human fetal pancreas

1989 ◽  
Vol 257 (2) ◽  
pp. C240-C251 ◽  
Author(s):  
M. A. Gray ◽  
A. Harris ◽  
L. Coleman ◽  
J. R. Greenwell ◽  
B. E. Argent
Keyword(s):  
Chloride Channel ◽  
State Probability ◽  
Apical Plasma Membrane ◽  
Patch Clamp Technique ◽  
Fetal Pancreas ◽  
Duct Cells ◽  
Human Fetal Pancreas ◽  
Outward Rectification ◽  
Voltage Dependent ◽  
Cells Cultured

Using the patch-clamp technique, we have identified two types of chloride channel on duct cells cultured from human fetal pancreas. The channel we observed most frequently exhibited slight outward rectification, had a conductance of 4-7 pS in cell-attached patches, and was present on the apical plasma membrane where it usually occurred in clusters. Its open-state probability was not markedly voltage dependent but was increased up to threefold by exposing duct cells to secretin (10 nM), dibutyryl cyclic AMP (1 mM), or forskolin (1 microM). The other type of chloride channel was only rarely observed. Its current-voltage relationship exhibited marked outward rectification, giving chord conductances of 19 pS for inward currents and 53 pS for outward currents. Although this channel could be activated by sustained depolarization of excised patches, once activated the open state probability was not voltage dependent. While the physiological role of these channels is not firmly established, the small-conductance channel might function in parallel with a Cl- -HCO-3 exchanger to provide a mechanism for electrogenic bicarbonate secretion from the duct cell.

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