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Chloride intracellular channel 1 (CLIC1): Sensor and effector during oxidative stress
Author(s) -
Averaimo Stefania,
Milton Rosemary H.,
Duchen Michael R.,
Mazzanti Michele
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.02.073
Subject(s) - nicotinamide adenine dinucleotide phosphate , nadph oxidase , chemistry , oxidative stress , cytosol , reactive oxygen species , intracellular , chloride channel , microbiology and biotechnology , superoxide , biochemistry , biophysics , oxidative phosphorylation , extracellular , oxidase test , enzyme , biology
Oxidative stress, characterized by overproduction of reactive oxygen species (ROS), is a major feature of several pathological states. Indeed, many cancers and neurodegenerative diseases are accompanied by altered redox balance, which results from dysregulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this review, we consider the role of the intracellular chloride channel 1 (CLIC1) in microglial cells during oxidative stress. Following microglial activation, CLIC1 translocates from the cytosol to the plasma membrane where it promotes a chloride conductance. The resultant anionic current balances the excess charge extruded by the active NADPH oxidase, supporting the generation of superoxide by the enzyme. In this scenario, CLIC1 could be considered to act as both a second messenger and an executor.