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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

articles

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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In vivo activation of the cystic fibrosis transmembrane conductance regulator mutant Delta F508 in murine nasal epithelium.
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B. N. Ling, J. B. Zuckerman, C. Lin, B. J. Harte, K. A. McNulty, P. R. Smith, L. M. Gomez, R. T. Worrell, D. C. Eaton, and T. R. Kleyman (1997)
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Altered fluid transport across airway epithelium in cystic fibrosis.
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A multifunctional aqueous channel formed by CFTR.
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Science 258, 1477-1479
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J. N. Snouwaert, K. K. Brigman, A. M. Latour, N. N. Malouf, R. C. Boucher, O. Smithies, and B. H. Koller (1992)
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Cystic fibrosis: molecular biology and therapeutic implications.
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Science 256, 774-779
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Science 256, 444-445
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