Journal
NATURE
Volume 440, Issue 7083, Pages 477-483Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature04712
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Funding
- Medical Research Council [G0501200] Funding Source: Medline
- NIDDK NIH HHS [R01 DK051767, R01 DK051767-10] Funding Source: Medline
- MRC [G0501200] Funding Source: UKRI
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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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