34 results on '"Brengman, Joan M"'
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2. Phenotypic heterogeneity in a large Thai slow-channel congenital myasthenic syndrome kinship
3. Congenital Myasthenic Syndrome Caused by Prolonged Acetylcholine Receptor Channel Openings Due to a Mutation in the M2 Domain of the ε Subunit
4. Myasthenic syndrome AChR α C-loop mutant disrupts initiation of channel gating
5. Myasthenic syndrome AChRα C-loop mutant disrupts initiation of channel gating
6. Paraneoplastic cerebellar degeneration with a circulating antibody against neurons and non-neuronal cells
7. Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit
8. E-box mutations in the RAPSN promoter region in eight cases with congenital myasthenic syndrome
9. Mutation causing severe myasthenia reveals functional asymmetry of AChR signature cystine loops in agonist binding and gating
10. Fundamental Gating Mechanism of Nicotinic Receptor Channel Revealed by Mutation Causing a Congenital Myasthenic Syndrome
11. Mutation causing congenital myasthenia reveals acetylcholine receptor β/δ subunit interaction essential for assembly
12. Frameshifting and Splice-Site Mutations in the Acetylcholine Receptor ϵ Subunit Gene in Three Turkish Kinships with Congenital Myasthenic Syndromesa
13. AChR Channel Blockade by Quinidine Sulfate Reduces Channel Open Duration in the Slow-Channel Congenital Myasthenic Syndromea
14. Congenital End-Plate Acetylcholinesterase Deficiency Caused by a Nonsense Mutation and an A→G Splice-Donor–Site Mutation at Position +3 of the Collagenlike-Tail–Subunit Gene ( COLQ): How Does G at Position +3 Result in Aberrant Splicing?
15. Mutations causing congenital myasthenia reveal principal coupling pathway in the acetylcholine receptor ε-subunit
16. Immunohistochemical Investigation of Ischemic and Postischemic Damage After Bilateral Carotid Occlusion in Gerbils
17. Prediction of Stroke Before and After Unilateral Occlusion of the Common Carotid Artery in Gerbils
18. The spectrum of mutations causing end-plate acetylcholinesterase deficiency
19. Myasthenic syndromes in Turkish kinships due to mutations in the acetylcholine receptor
20. Quinidine normalizes the open duration of slow-channel mutants of the acetylcholine receptor
21. Mode Switching Kinetics Produced by a Naturally Occurring Mutation in the Cytoplasmic Loop of the Human Acetylcholine Receptor ε Subunit
22. Congenital Myasthenic Syndrome Caused by Decreased Agonist Binding Affinity Due to a Mutation in the Acetylcholine Receptor ε Subunit
23. Analysis of cytokine expression in muscle in inflammatory myopathies, Duchenne dystrophy, and non-weak controls
24. Highly fatal fast-channel syndrome caused by AChR ε subunit mutation at the agonist binding site.
25. Highly fatal fast-channel syndrome caused by AChR ε subunit mutation at the agonist binding site.
26. Highly fatal fast-channel syndrome caused by AChR [Latin Small Letter Open E] subunit mutation at the agonist binding site
27. Congenital Myasthenic Syndromes due to Heteroallelic Nonsense/Missense Mutations in the Acetylcholine Receptor ε Subunit Gene: Identification and Functional Characterization of Six New Mutations.
28. New Mutations in Acetylcholine Receptor Subunit Genes Reveal Heterogeneity in the Slow-Channel Congenital Myasthenic Syndrome.
29. AChR Channel Blockade by Quinidine Sulfate Reduces Channel Open Duration in the Slow-Channel Congenital Myasthenic Syndromea.
30. Frameshifting and Splice-Site Mutations in the Acetylcholine Receptor ɛ Subunit Gene in Three Turkish Kinships with Congenital Myasthenic Syndromesa.
31. Frameshifting and Splice-Site Mutations in the Acetylcholine Receptor Subunit Gene in Three Turkish Kinships with Congenital Myasthenic Syndromes a
32. Quinidine normalizes the open duration of slowchannel mutants of the acetylcholine receptor
33. Immunohistochemical investigation of cerebral ischemia during recirculation
34. Mutation causing severe myasthenia reveals functional asymmetry of AChR signature cystine loops in agonist binding and gating.
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