ArticleThe Journal of general physiology2003
Voltage-dependent gating of the cystic fibrosis transmembrane conductance regulator Cl- channel.
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 34 papers.
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Who cites it
34 citing papers in PubMed.
- Two rare variants that affect the same amino acid in CFTR have distinct responses to ivacaftor.The Journal of physiology · 2024Article
- Estimating the true stability of the prehydrolytic outward-facing state in an ABC protein.eLife · 2023Article
- Optimization of CFTR gating through the evolution of its extracellular loops.The Journal of general physiology · 2023Article
- Molecular pathology of the R117H cystic fibrosis mutation is explained by loss of a hydrogen bond.eLife · 2021Article
- Differential thermostability and response to cystic fibrosis transmembrane conductance regulator potentiators of human and mouse F508del-CFTR.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Thermodynamic secrets of multidrug resistance: A new take on transport mechanisms of secondary active antiporters.Protein science : a publication of the Protein Society · 2018Review
- CFTR is involved in the regulation of glucagon secretion in human and rodent alpha cells.Scientific reports · 2017Article
- Altering intracellular pH reveals the kinetic basis of intraburst gating in the CFTR ClThe Journal of physiology · 2017Article
- The gating of the CFTR channel.Cellular and molecular life sciences : CMLS · 2017Review
- Molecular modelling and molecular dynamics of CFTR.Cellular and molecular life sciences : CMLS · 2017Review
- Article
- Impact of the F508del mutation on ovine CFTR, a Cl- channel with enhanced conductance and ATP-dependent gating.The Journal of physiology · 2015Article
- Cysteine accessibility probes timing and extent of NBD separation along the dimer interface in gating CFTR channels.The Journal of general physiology · 2015Article
- Loop diuretics are open-channel blockers of the cystic fibrosis transmembrane conductance regulator with distinct kinetics.British journal of pharmacology · 2014Article
- The silent codon change I507-ATC->ATT contributes to the severity of the ΔF508 CFTR channel dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Acute inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel by thyroid hormones involves multiple mechanisms.American journal of physiology. Cell physiology · 2013Article
- Conformational changes in the catalytically inactive nucleotide-binding site of CFTR.The Journal of general physiology · 2013Article
- Cystic fibrosis transmembrane conductance regulator (ABCC7) structure.Cold Spring Harbor perspectives in medicine · 2013Review
- Locating a plausible binding site for an open-channel blocker, GlyH-101, in the pore of the cystic fibrosis transmembrane conductance regulator.Molecular pharmacology · 2012Article
- Lubiprostone activates CFTR, but not ClC-2, via the prostaglandin receptor (EP(4)).Biochemical and biophysical research communications · 2012Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When excised inside-out membrane patches are bathed in symmetrical Cl--rich solutions, the current-voltage (I-V) relationship of macroscopic cystic fibrosis transmembrane conductance regulator (CFTR) Cl- currents inwardly rectifies at large positive voltages. To investigate the mechanism of inward rectification, we studied CFTR Cl- channels in excised inside-out membrane patches from cells expressing wild-type human and murine CFTR using voltage-ramp and -step protocols. Using a voltage-ramp protocol, the magnitude of human CFTR Cl- current at +100 mV was 74 +/- 2% (n = 10) of that at -100 mV. This rectification of macroscopic CFTR Cl- current was reproduced in full by ensemble currents generated by averaging single-channel currents elicited by an identical voltage-ramp protocol. However, using a voltage-step protocol the single-channel current amplitude (i) of human CFTR at +100 mV was 88 +/- 2% (n = 10) of that at -100 mV. Based on these data, we hypothesized that voltage might alter the gating behavior of human CFTR. Using linear three-state kinetic schemes, we demonstrated that voltage has marked effects on channel gating. Membrane depolarization decreased both the duration of bursts and the interburst interval, but increased the duration of gaps within bursts. However, because the voltage dependencies of the different rate constants were in opposite directions, voltage was without large effect on the open probability (Po) of human CFTR. In contrast, the Po of murine CFTR was decreased markedly at positive voltages, suggesting that the rectification of murine CFTR is stronger than that of human CFTR. We conclude that inward rectification of CFTR is caused by a reduction in i and changes in gating kinetics. We suggest that inward rectification is an intrinsic property of the CFTR Cl- channel and not the result of pore block.
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