Steven M. Sine mainly focuses on Acetylcholine receptor, Receptor, Biophysics, CHRNE and Agonist. His Acetylcholine receptor research is multidisciplinary, incorporating perspectives in Endocrinology, Acetylcholine and Protein subunit. The Receptor study which covers Neuroscience that intersects with Signal transduction.
The concepts of his Biophysics study are interwoven with issues in Muscarinic acetylcholine receptor M5, Nicotinic agonist, Stereochemistry and Ion channel. His studies in Stereochemistry integrate themes in fields like Binding site and Dissociation constant. His CHRNE study integrates concerns from other disciplines, such as HEK 293 cells, Molecular biology, Cell biology and RAPSN.
Steven M. Sine mostly deals with Acetylcholine receptor, Receptor, Biophysics, Protein subunit and Stereochemistry. His biological study spans a wide range of topics, including Agonist, Mutation, Acetylcholine, Nicotinic agonist and Neuroscience. His work on Dissociation constant, Transmembrane protein and Neurotransmitter binding as part of general Receptor study is frequently linked to Cysteine, bridging the gap between disciplines.
Steven M. Sine interconnects Biochemistry, Ion channel and Molecular dynamics in the investigation of issues within Biophysics. His Protein subunit research includes themes of Mutant, Point mutation and Cell biology. His Stereochemistry research is multidisciplinary, incorporating elements of Acetylcholine binding, Nicotinic acetylcholine receptor, Binding site and Ligand.
His primary areas of study are Biophysics, Acetylcholine receptor, Receptor, Nicotinic agonist and Protein subunit. His Biophysics study combines topics from a wide range of disciplines, such as Agonist, Ethanol, Extracellular and Acetylcholine. His Acetylcholine receptor research integrates issues from Gating, Mutant and Cholinergic.
His work in Receptor addresses issues such as Binding site, which are connected to fields such as Protein structure and Bungarotoxin. The Nicotinic agonist study combines topics in areas such as Long-term potentiation and Patch clamp. His Protein subunit research incorporates elements of Allosteric regulation and Cell biology.
Acetylcholine receptor, Nicotinic agonist, Receptor, Biophysics and Agonist are his primary areas of study. His Acetylcholine receptor research is multidisciplinary, incorporating elements of Protein subunit, Bioinformatics and Pathology. His studies examine the connections between Protein subunit and genetics, as well as such issues in Protein structure, with regards to Binding site, Epibatidine and Plasma protein binding.
His studies in Nicotinic agonist integrate themes in fields like Patch clamp, Stereochemistry and Ion channel. Steven M. Sine specializes in Receptor, namely Cys-loop receptors. Particularly relevant to Gating is his body of work in Biophysics.
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Data transformations for improved display and fitting of single-channel dwell time histograms
F.J. Sigworth;S.M. Sine.
Biophysical Journal (1987)
Recent advances in Cys-loop receptor structure and function.
Steven M. Sine;Andrew G. Engel.
Congenital myasthenic syndromes: pathogenesis, diagnosis, and treatment.
Andrew G. Engel;Xin Ming Shen;Duygu Selcen;Steven M. Sine.
Lancet Neurology (2015)
Principal pathway coupling agonist binding to channel gating in nicotinic receptors
Won Yong Lee;Steven M. Sine.
Coupling of agonist binding to channel gating in an ACh-binding protein linked to an ion channel
Cecilia Beatriz Bouzat;Fernanda Andrea Gumilar;Guillermo Federico Spitzmaul;Hai Long Wang.
Mutation of the acetylcholine receptor α subunit causes a slow-channel myasthenic syndrome by enhancing agonist binding affinity
Steven M. Sine;Kinji Ohno;Cecilia Bouzat;Anthony Auerbach.
Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit.
Kinji Ohno;David O. Hutchinson;Margherita Milone;Joan M. Brengman.
Proceedings of the National Academy of Sciences of the United States of America (1995)
Activation of Torpedo acetylcholine receptors expressed in mouse fibroblasts. Single channel current kinetics reveal distinct agonist binding affinities.
Steven M. Sine;Toni Claudio;Fred J. Sigworth.
The Journal of General Physiology (1990)
Congenital Myasthenic Syndrome Caused by Decreased Agonist Binding Affinity Due to a Mutation in the Acetylcholine Receptor ε Subunit
Kinji Ohno;Hai Long Wang;Margherita Milone;Nina Bren.
New Mutations in Acetylcholine Receptor Subunit Genes Reveal Heterogeneity in the Slow-Channel Congenital Myasthenic Syndrome
Andrew G. Engel;Kinji Ohno;Margherita Milone;Hai Long Wang.
Human Molecular Genetics (1996)
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