ArticleThe Journal of physiology1999
A re-examination of adult mouse nicotinic acetylcholine receptor channel activation kinetics.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 103 citations in OpenAlex.
- MscS inactivation and recovery are slow voltage-dependent processes sensitive to interactions with lipids.Biophysical journal · 2024Article
- α3β4 Acetylcholine Nicotinic Receptors Are Components of the Secretory Machinery Clusters in Chromaffin Cells.International journal of molecular sciences · 2022Article
- Efficiency measures the conversion of agonist binding energy into receptor conformational change.The Journal of general physiology · 2019Article
- Molecular recognition at cholinergic synapses: acetylcholine versus choline.The Journal of physiology · 2017Article
- A mechanism for acetylcholine receptor gating based on structure, coupling, phi, and flip.The Journal of general physiology · 2017Article
- Structural correlates of affinity in fetal versus adult endplate nicotinic receptors.Nature communications · 2016Article
- Dose-Response Analysis When There Is a Correlation between Affinity and Efficacy.Molecular pharmacology · 2016Article
- Poly(ethylene glycol) as a scaffold for high-affinity open-channel blockers of the mouse nicotinic acetylcholine receptor.PloS one · 2014Article
- Energy for wild-type acetylcholine receptor channel gating from different choline derivatives.Biophysical journal · 2013Article
- Perspectives on: conformational coupling in ion channels: allosteric coupling in ligand-gated ion channels.The Journal of general physiology · 2012Article
- The intrinsic energy of the gating isomerization of a neuromuscular acetylcholine receptor channel.The Journal of general physiology · 2012Article
- The energetic consequences of loop 9 gating motions in acetylcholine receptor-channels.The Journal of physiology · 2012Article
- Glycine hinges with opposing actions at the acetylcholine receptor-channel transmitter binding site.Molecular pharmacology · 2011Article
- Temperature dependence of acetylcholine receptor channels activated by different agonists.Biophysical journal · 2011Article
- Linking the acetylcholine receptor-channel agonist-binding sites with the gate.Biophysical journal · 2010Article
- Acetylcholine receptor channels activated by a single agonist molecule.Biophysical journal · 2010Article
- Structural basis of activation of cys-loop receptors: the extracellular-transmembrane interface as a coupling region.Molecular neurobiology · 2009Review
- The local anaesthetics proadifen and adiphenine inhibit nicotinic receptors by different molecular mechanisms.British journal of pharmacology · 2009Article
- Energy and structure of the M2 helix in acetylcholine receptor-channel gating.Biophysical journal · 2009Article
- Decremental response to high-frequency trains of acetylcholine pulses but unaltered fractional Ca2+ currents in a panel of "slow-channel syndrome" nicotinic receptor mutants.The Journal of general physiology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. During routine sequencing of our mouse muscle alpha subunit acetylcholine receptor channel (AChR) cDNA clones, we detected a discrepancy with the GenBank database entry (accession X03986). At nucleotides 1305-7 (residue 433, in the M4 domain) the database lists GTC which encodes a valine, while our putative 'wild-type' cDNA had the nucleotides GCC, which encodes an alanine. No other sequence differences were found. 2. PCR amplification of genomic DNA confirmed that the BALB/C mouse alpha subunit gene has a T nucleotide at position 1306, and, therefore, that the protein has a V at position 433 in the M4 segment. 3. In order to determine the functional consequences of this difference, either wild-type (V433) or mutant (A433) alpha subunits were co-expressed in HEK cells with mouse beta, epsilon and delta subunits. Single-channel currents were recorded in cell-attached patches, and rate and equilibrium constants were estimated from open and closed durations obtained from a range of ACh concentrations. No significant differences were found between the activation rate constants or equilibrium constants of the V433 and A433 variants. 4. Kinetic modelling of alphaV433 AChR suggests that the two transmitter binding sites have similar dissociation equilibrium constants for acetylcholine ( approximately 160 microM in 142 mM extracellular KCl). 5. Diliganded AChRs occupy a closed state that has a lifetime of approximately 1 ms. The rate constants for entering and leaving this state do not vary with the ACh concentration. 6. The kinetics of a mutant AChR that causes a slow channel congenital myaesthenic syndrome, alphaG153S, was re-examined. The properties of this mutant were similar with a V or an A at position alpha433.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.