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Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Physiol 2015 ; 593 (Pt 18): 4091-109 Nephropedia Template TP
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Discovery of CLC transport proteins: cloning, structure, function and pathophysiology #MMPMID25590607
Jentsch TJ
J Physiol 2015[Sep]; 593 (Pt 18): 4091-109 PMID25590607show ga
After providing a personal description of the convoluted path leading 25 years ago to the molecular identification of the Torpedo Cl? channel ClC-0 and the discovery of the CLC gene family, I succinctly describe the general structural and functional features of these ion transporters before giving a short overview of mammalian CLCs. These can be categorized into plasma membrane Cl? channels and vesicular Cl?/H+-exchangers. They are involved in the regulation of membrane excitability, transepithelial transport, extracellular ion homeostasis, endocytosis and lysosomal function. Diseases caused by CLC dysfunction include myotonia, neurodegeneration, deafness, blindness, leukodystrophy, male infertility, renal salt loss, kidney stones and osteopetrosis, revealing a surprisingly broad spectrum of biological roles for chloride transport that was unsuspected when I set out to clone the first voltage-gated chloride channel.