ArticleThe Journal of general physiology2003
Mutation-induced blocker permeability and multiion block of the CFTR chloride channel pore.
Article in The Journal of general physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Molecular structure of the ATP-bound, phosphorylated human CFTR.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cystic Fibrosis Transmembrane Conductance Regulator (CFTR): CLOSED AND OPEN STATE CHANNEL MODELS.The Journal of biological chemistry · 2015Article
- State-dependent blocker interactions with the CFTR chloride channel: implications for gating the pore.Pflugers Archiv : European journal of physiology · 2014Article
- Cystic fibrosis transmembrane conductance regulator chloride channel blockers: Pharmacological, biophysical and physiological relevance.World journal of biological chemistry · 2014Review
- Pseudohalide anions reveal a novel extracellular site for potentiators to increase CFTR function.British journal of pharmacology · 2012Article
- Tuning of CFTR chloride channel function by location of positive charges within the pore.Biophysical journal · 2012Article
- Sialin (SLC17A5) functions as a nitrate transporter in the plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Differential contribution of TM6 and TM12 to the pore of CFTR identified by three sulfonylurea-based blockers.Pflugers Archiv : European journal of physiology · 2012Article
- Divergent CFTR orthologs respond differently to the channel inhibitors CFTRinh-172, glibenclamide, and GlyH-101.American journal of physiology. Cell physiology · 2012Article
- Functional differences in pore properties between wild-type and cysteine-less forms of the CFTR chloride channel.The Journal of membrane biology · 2011Article
- Functional arrangement of the 12th transmembrane region in the CFTR chloride channel pore based on functional investigation of a cysteine-less CFTR variant.Pflugers Archiv : European journal of physiology · 2011Article
- Alignment of transmembrane regions in the cystic fibrosis transmembrane conductance regulator chloride channel pore.The Journal of general physiology · 2011Article
- Anion currents in yeast K+ transporters (TRK) characterize a structural homologue of ligand-gated ion channels.Pflugers Archiv : European journal of physiology · 2011Article
- Changes in accessibility of cytoplasmic substances to the pore associated with activation of the cystic fibrosis transmembrane conductance regulator chloride channel.The Journal of biological chemistry · 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
- Novel residues lining the CFTR chloride channel pore identified by functional modification of introduced cysteines.The Journal of membrane biology · 2009Article
- Identification of positive charges situated at the outer mouth of the CFTR chloride channel pore.Pflugers Archiv : European journal of physiology · 2008Article
- Direct and indirect effects of mutations at the outer mouth of the cystic fibrosis transmembrane conductance regulator chloride channel pore.The Journal of membrane biology · 2007Article
- On the origin of asymmetric interactions between permeant anions and the cystic fibrosis transmembrane conductance regulator chloride channel pore.Biophysical journal · 2007Article
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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
Chloride permeation through the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel is blocked by a broad range of anions that bind tightly within the pore. Here we show that the divalent anion Pt(NO2)42- acts as an impermeant voltage-dependent blocker of the CFTR pore when added to the intracellular face of excised membrane patches. Block was of modest affinity (apparent Kd 556 microM), kinetically fast, and weakened by extracellular Cl- ions. A mutation in the pore region that alters anion selectivity, F337A, but not another mutation at the same site that has no effect on selectivity (F337Y), had a complex effect on channel block by intracellular Pt(NO2)42- ions. Relative to wild-type, block of F337A-CFTR was weakened at depolarized voltages but strengthened at hyperpolarized voltages. Current in the presence of Pt(NO2)42- increased at very negative voltages in F337A but not wild-type or F337Y, apparently due to relief of block by permeation of Pt(NO2)42- ions to the extracellular solution. This "punchthrough" was prevented by extracellular Cl- ions, reminiscent of a "lock-in" effect. Relief of block in F337A by Pt(NO2)42- permeation was only observed for blocker concentrations above 300 microM; as a result, block at very negative voltages showed an anomalous concentration dependence, with an increase in blocker concentration causing a significant weakening of block and an increase in Cl- current. We interpret this effect as reflecting concentration-dependent permeability of Pt(NO2)42- in F337A, an apparent manifestation of an anomalous mole fraction effect. We suggest that the F337A mutation allows intracellular Pt(NO2)42- to enter deeply into the CFTR pore where it interacts with multiple binding sites, and that simultaneous binding of multiple Pt(NO2)42- ions within the pore promotes their permeation to the extracellular solution.
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