ArticleBritish journal of pharmacology1999
Substrates of multidrug resistance-associated proteins block the cystic fibrosis transmembrane conductance regulator chloride channel.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- The molecular evolution of function in the CFTR chloride channel.The Journal of general physiology · 2021Article
- Increased Expression of Plasma-Induced ABCC1 mRNA in Cystic Fibrosis.International journal of molecular sciences · 2017Article
- Cystic fibrosis transmembrane conductance regulator chloride channel blockers: Pharmacological, biophysical and physiological relevance.World journal of biological chemistry · 2014Review
- ATP hydrolysis-dependent asymmetry of the conformation of CFTR channel pore.The journal of physiological sciences : JPS · 2011Article
- MRP transporters as membrane machinery in the bradykinin-inducible export of ATP.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Regulation of conductance by the number of fixed positive charges in the intracellular vestibule of the CFTR chloride channel pore.The Journal of general physiology · 2010Article
- Cysteine-independent inhibition of the CFTR chloride channel by the cysteine-reactive reagent sodium (2-sulphonatoethyl) methanethiosulphonate.British journal of pharmacology · 2009Article
- Block of CFTR-dependent chloride currents by inhibitors of multidrug resistance-associated proteins.European journal of pharmacology · 2007Article
- Interactions between impermeant blocking ions in the cystic fibrosis transmembrane conductance regulator chloride channel pore: evidence for anion-induced conformational changes.The Journal of membrane biology · 2006Article
- ATP-binding cassette (ABC) transporters in normal and pathological lung.Respiratory research · 2005Review
- Mutation-induced blocker permeability and multiion block of the CFTR chloride channel pore.The Journal of general physiology · 2003Article
- Voltage-dependent gating of the cystic fibrosis transmembrane conductance regulator Cl- channel.The Journal of general physiology · 2003Article
- Coupled movement of permeant and blocking ions in the CFTR chloride channel pore.The Journal of physiology · 2003Article
- Mechanism of lonidamine inhibition of the CFTR chloride channel.British journal of pharmacology · 2002Article
- Multiple inhibitory effects of Au(CN)(2-) ions on cystic fibrosis transmembrane conductance regulator Cl(-) channel currents.The Journal of physiology · 2002Article
- Plasma membrane glutathione transporters and their roles in cell physiology and pathophysiology.Molecular aspects of medicineReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of physiological substrates of multidrug resistance-associated proteins (MRPs) on cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel currents were examined using patch clamp recording from CFTR-transfected mammalian cell lines. 2. Two MRP substrates, taurolithocholate-3-sulphate (TLCS) and beta-estradiol 17-(beta-D-glucuronide) (E217betaG) caused a voltage-dependent block of macroscopic CFTR Cl- currents when applied to the intracellular face of excised membrane patches, with mean apparent dissociation constants (KDs) of 96+/-10 and 563+/-103 microM (at 0 mV) respectively. The unconjugated bile salts taurocholate and cholate were also effective CFTR channel blockers under these conditions, with KDs of 453+/-44 and 3760+/-710 microM (at 0 mV) respectively. 3. Reducing the extracellular Cl- concentration from 154 to 20 mM decreased the KD for block intracellular TLCS to 54+/-1 microM, and also significantly reduced the voltage dependence of block, by suggesting that TLCS blocks Cl- permeation through CFTR by binding within the channel pore. 4. Intracellular TLCS reduced the apparent amplitude of CFTR single channel currents, suggesting that the duration of block is very fast compared to the gating of the channel. 5. The apparent affinity of block by TLCs is comparable to that of other well-known CFTR channel blockers, suggesting that MRP substrates may comprise a novel class of probes of the CFTR channel pore. 6. These results also suggest that the related proteins CFTR and MRP may share a structurally similar anion binding site at the cytoplasmic face of the membrane.
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