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Nature 440, 477-483 (23 March 2006) | doi:10.1038/nature04712; Published online 22 March 2006
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Review Article The ABC protein turned chloride channel whose failure causes cystic fibrosis
David C. Gadsby1, Paola Vergani2 & László Csanády3
Abstract
CFTR chloride channels are encoded by the gene mutated in patients with cystic fibrosis. These channels belong to the superfamily of ABC transporter ATPases. ATP-driven conformational changes, which in other ABC proteins fuel uphill substrate transport across cellular membranes, in CFTR open and close a gate to allow transmembrane flow of anions down their electrochemical gradient. New structural and biochemical information from prokaryotic ABC proteins and functional information from CFTR channels has led to a unifying mechanism explaining those ATP-driven conformational changes.
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