Slow-Channel Myasthenic Syndrome Caused By Enhanced Activation, Desensitization, and Agonist Binding Affinity Attributable to Mutation in the M2 Domain of the Acetylcholine Receptor α Subunit

Lignende værker

• Rapsyn Mutations in Humans Cause Endplate Acetylcholine-Receptor Deficiency and Myasthenic Syndrome
  af: Ohno, Kinji, et al.
  Udgivet: (2002)
• Mutation in the M1 Domain of the Acetylcholine Receptor α Subunit Decreases the Rate of Agonist Dissociation
  af: Wang, Hai-Long, et al.
  Udgivet: (1997)
• Mutation causing congenital myasthenia reveals acetylcholine receptor β/δ subunit interaction essential for assembly
  af: Quiram, Polly A., et al.
  Udgivet: (1999)
• Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit.
  af: Ohno, K, et al.
  Udgivet: (1995)
• Serum choline activates mutant acetylcholine receptors that cause slow channel congenital myasthenic syndromes
  af: Zhou, Ming, et al.
  Udgivet: (1999)