Interaction between calcium-activated chloride channels and the cystic fibrosis transmembrane conductance regulator
| Autor: | Bernd Nilius, Jean-Jacques Cassiman, Guillaume Droogmans, Harry Cuppens, Jan Eggermont, Lin Wei, Anne Vankeerberghen |
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| Rok vydání: | 1999 |
| Předmět: |
congenital
hereditary and neonatal diseases and abnormalities medicine.medical_specialty Physiology Clinical Biochemistry Cystic Fibrosis Transmembrane Conductance Regulator Gene Expression Pulmonary Artery Transfection Cystic fibrosis Cell Line chemistry.chemical_compound Chloride Channels Internal medicine 1-Methyl-3-isobutylxanthine Physiology (medical) medicine Animals ΔF508 Forskolin biology Endoplasmic reticulum Sodium channel Cell Membrane Colforsin Electric Conductivity respiratory system medicine.disease digestive system diseases Cystic fibrosis transmembrane conductance regulator respiratory tract diseases Cell biology Endocrinology chemistry Mutation Chloride channel biology.protein Calcium Cattle Endothelium Vascular |
| Zdroj: | Pfl�gers Archiv European Journal of Physiology. 438:635-641 |
| ISSN: | 1432-2013 0031-6768 |
| DOI: | 10.1007/s004240051087 |
| Popis: | We investigated interactions between cystic fibrosis conductance regulator (CFTR) and endogenous Ca2+-activated Cl- channels (CaCC) in bovine pulmonary artery endothelium (CPAE). CPAE cells, which do not express CFTR, were transiently transfected with wild-type (WT) CFTR and the deletion mutant deltaF508 CFTR. Currents through CaCC were significantly reduced after expression of WT CFTR. This inhibition was increased by stimulation (isobutylmethylxanthine, forskolin) of CFTR in cells expressing WT CFTR. There were no such effects when deltaF508 mutant CFTR, which is retained in the endoplasmic reticulum, was expressed. It is concluded that CFTR and CaCC are functionally coupled probably through a direct channel-channel interaction. |
| Databáze: | OpenAIRE |
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