Abstract
The transient receptor potential canonical type-3 (TRPC3, receptor- and store-operated Ca 2+ influx channel) participates in skeletal muscle contraction; its functional interactions with ryanodine receptor-1 (RyR1) are independent of sarcoplasmic Ca 2+ content and dihydropyridine receptor. In 25 generalized myasthenia gravis (MG), we detected antibodies against human TRPC3 peptide in 9 patients (8 with thymoma and one with hyperplastic thymus) and those against human RyR1 peptides in 16 patients (15 with thymoma and one with hyperplastic thymus). Both antibodies were found in patients with more severe myasthenia and could contribute to the contractile abnormalities in MG.
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