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lüll The emerging diversity of neuromuscular junction disorders Newsom-Davis JActa Myol 2007[Jul]; 26 (1): 5-10Research advances over the last 30 years have shown that key transmembrane proteins at the neuromuscular junction are vulnerable to antibody-mediated autoimmune attack These targets are acetylcholine receptors (AChRs) and muscle specific kinase (MuSK) in myasthenia gravis, voltage-gated calcium channels (VGCCs) in the Lambert-Eaton myasthenic syndrome (LEMS), and voltage-gated potassium channels (VGKCs) in neuromyotonia. In parallel with these immunological advances, mutations identified in genes encoding pre-synaptic, synaptic and postsynaptic proteins that are crucial to neuromuscular transmission have revealed a similar diversity of congenital myasthenic syndromes (CMS). These discoveries have had a major impact on diagnosis and management.|Female[MESH]|Humans[MESH]|Infant, Newborn[MESH]|Lambert-Eaton Myasthenic Syndrome/physiopathology[MESH]|Myasthenia Gravis, Neonatal/genetics[MESH]|Myasthenia Gravis/genetics/*physiopathology[MESH]|Neuromuscular Diseases/*classification/physiopathology[MESH]|Neuromuscular Junction/*physiopathology[MESH]|Pregnancy[MESH]|Pregnancy Complications/physiopathology[MESH] |