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Science 24 April 1992: Vol. 256. no. 5056, pp. 530 - 532 DOI: 10.1126/science.1373908
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Articles
Science, Vol 256, Issue 5056, 530-532
Copyright © 1992 by American Association for the Advancement of Science
Regulation of plasma membrane recycling by CFTR
NA Bradbury,
T Jilling,
G Berta,
EJ Sorscher,
RJ Bridges,
and
KL Kirk
Department of Physiology and Biophysics, University of Alabama, Birmingham 35294.
The gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) is defective in patients with cystic fibrosis. Although the protein product of the CFTR gene has been proposed to function as a chloride ion channel, certain aspects of its function remain unclear. The role of CFTR in the adenosine 3',5'-monophosphate (cAMP)-dependent regulation of plasma membrane recycling was examined. Adenosine 3',5'-monophosphate is known to regulate endocytosis and exocytosis in chloride-secreting epithelial cells that express CFTR. However, mutant epithelial cells derived from a patient with cystic fibrosis exhibited no cAMP-dependent regulation of endocytosis and exocytosis until they were transfected with complementary DNA encoding wild-type CFTR. Thus, CFTR is critical for cAMP-dependent regulation of membrane recycling in epithelial tissues, and this function of CFTR could explain in part the pleiotropic nature of cystic fibrosis.
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