MECHANISMS UNDERLYING REGULATED CFTR TRAFFICKING - 06/09/11
Résumé |
The cystic fibrosis transmembrane conductance regulator (CFTR) is a phosphorylation and nucleotide regulated anion channel that accounts for the cyclic adenosine monophosphate (cAMP)–stimulated chloride (Cl) conductance at the apical membranes of many secretory epithelial cells. The mechanisms regulating CFTR channel gating have been well documented, principally from studies in heterologous expression systems.14 In addition to regulation of CFTR's open probability, cAMP/protein kinase A (PKA) also regulate the insertion and retrieval of CFTR at the plasma membrane and acutely control the density of CFTR channels that can contribute to the apical Cl conductance. Evidence supporting the concept of CFTR-dependent membrane trafficking includes measurements of endocytic marker uptake into CFTR-expressing cells3 and the identification of CFTR in clathrin-coated membrane vesicles, which indicates that CFTR is retrieved.2 Parallel measurements of Cl conductance and membrane capacitance indicate that cells increase their surface area during CFTR and cAMP-dependent Cl current stimulation.13, 16
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| Address reprint requests to Raymond A. Frizzell, PhD, Department of Cell Biology and Psysiology, 5362 BST, 3500 Terrace Street, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261 |
Vol 84 - N° 3
P. 633-640 - mai 2000 Retour au numéro
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