ArticleProceedings of the National Academy of Sciences of the United States of America1999
Serum choline activates mutant acetylcholine receptors that cause slow channel congenital myasthenic syndromes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 86 citations in OpenAlex.
- Positive allosteric modulator selective for adult muscle nicotinic acetylcholine receptor.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Null method to estimate the maximal PA at subsaturating concentrations of agonist.The Journal of general physiology · 2025Article
- Agonist efficiency from concentration-response curves: Structural implications and applications.Biophysical journal · 2021Article
- Slow-channel myasthenia due to novel mutation in M2 domain of AChR delta subunit.Annals of clinical and translational neurology · 2019Article
- Efficiency measures the conversion of agonist binding energy into receptor conformational change.The Journal of general physiology · 2019Article
- Cyclic activation of endplate acetylcholine receptors.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mutations Causing Slow-Channel Myasthenia Reveal That a Valine Ring in the Channel Pore of Muscle AChR is Optimized for Stabilizing Channel Gating.Human mutation · 2016Article
- Investigation of Congenital Myasthenia Reveals Functional Asymmetry of Invariant Acetylcholine Receptor (AChR) Cys-loop Aspartates.The Journal of biological chemistry · 2016Article
- Activation of endplate nicotinic acetylcholine receptors by agonists.Biochemical pharmacology · 2015Review
- Conserved allosteric hot spots in the transmembrane domains of cystic fibrosis transmembrane conductance regulator (CFTR) channels and multidrug resistance protein (MRP) pumps.The Journal of biological chemistry · 2014Article
- Converting nonhydrolyzable nucleotides to strong cystic fibrosis transmembrane conductance regulator (CFTR) agonists by gain of function (GOF) mutations.The Journal of biological chemistry · 2013Article
- The energy and work of a ligand-gated ion channel.Journal of molecular biology · 2013Review
- Function of interfacial prolines at the transmitter-binding sites of the neuromuscular acetylcholine receptor.The Journal of biological chemistry · 2013Article
- Energy for wild-type acetylcholine receptor channel gating from different choline derivatives.Biophysical journal · 2013Article
- Action of nicotine and analogs on acetylcholine receptors having mutations of transmitter-binding site residue αG153.The Journal of general physiology · 2013Article
- A mechanistic description of gating of the human cardiac ryanodine receptor in a regulated minimal environment.The Journal of general physiology · 2012Article
- Acetylcholine receptor gating in a zebrafish model for slow-channel syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The intrinsic energy of the gating isomerization of a neuromuscular acetylcholine receptor channel.The Journal of general physiology · 2012Article
- Thinking in cycles: MWC is a good model for acetylcholine receptor-channels.The Journal of physiology · 2012Article
- Design and control of acetylcholine receptor conformational change.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We have found that mutant acetylcholine receptor channels (AChRs) that cause slow-channel congenital myasthenic syndromes are activated by serum and that the high frequency of openings in serum is reduced by treatment with choline oxidase. Thus, slow-channel congenital myasthenic syndrome AChRs at the neuromuscular junction are likely to be activated both by steady exposure to serum choline and by transient exposure to synaptically released transmitter. Single-channel kinetic analyses indicate that the increased response to choline is caused by a reduced intrinsic stability of the closed channel. The results suggest that a mutation that destabilizes the inactive conformation of the AChR, together with the sustained exposure of endplates to serum choline, results in continuous channel activity that contributes to the pathophysiology of the disease.
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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.