Electrodiffusional ATP movement through the cystic fibrosis transmembrane conductance regulator
Autor: | Claudio Grosman, Dennis A. Ausiello, George R. Jackson, I. L. Reisin, Horacio F. Cantiello, Catherine R. O'Riordan, Steven C. Borkan, A. G. Prat, Yihan Wang |
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Rok vydání: | 1998 |
Předmět: |
Models
Molecular congenital hereditary and neonatal diseases and abnormalities Physiology Lipid Bilayers Cystic Fibrosis Transmembrane Conductance Regulator Spodoptera Biology Cell Line Diffusion Adenosine Triphosphate Chlorides Chloride Channels Animals Humans Magnesium ortho-Aminobenzoates Nucleotide transport Electric Conductivity Biological Transport Cell Biology Calcium Channel Blockers Cyclic AMP-Dependent Protein Kinases Recombinant Proteins Cystic fibrosis transmembrane conductance regulator Transport protein Cell biology Biochemistry biology.protein |
Zdroj: | American Journal of Physiology-Cell Physiology. 274:C799-C809 |
ISSN: | 1522-1563 0363-6143 |
DOI: | 10.1152/ajpcell.1998.274.3.c799 |
Popis: | Expression of the cystic fibrosis transmembrane conductance regulator (CFTR), and of at least one other member of the ATP-binding cassette family of transport proteins, P-glycoprotein, is associated with the electrodiffusional movement of the nucleotide ATP. Evidence directly implicating CFTR expression with ATP channel activity, however, is still missing. Here it is reported that reconstitution into a lipid bilayer of highly purified CFTR of human epithelial origin enables the permeation of both Cl−and ATP. Similar to previously reported data for in vivo ATP currents of CFTR-expressing cells, the reconstituted channels displayed competition between Cl−and ATP and had multiple conductance states in the presence of Cl−and ATP. Purified CFTR-mediated ATP currents were activated by protein kinase A and ATP (1 mM) from the “intracellular” side of the molecule and were inhibited by diphenylamine-2-carboxylate, glibenclamide, and anti-CFTR antibodies. The absence of CFTR-mediated electrodiffusional ATP movement may thus be a relevant component of the pleiotropic cystic fibrosis phenotype. |
Databáze: | OpenAIRE |
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