Selective inhibition of caspases in skeletal muscle reverses the apoptotic synaptic degeneration in slow-channel myasthenic syndrome
Author:
Publisher
Oxford University Press (OUP)
Subject
Genetics(clinical),Genetics,Molecular Biology,General Medicine
Link
http://academic.oup.com/hmg/article-pdf/23/1/69/2141673/ddt397.pdf
Reference45 articles.
1. Congenital Myasthenic Syndromes: New Insights from Molecular Genetic and Patch-Clamp Studiesa
2. A newly recognized congenital myasthenic syndrome attributed to a prolonged open time of the acetylcholine-induced ion channel
3. Novel delta subunit mutation in slow-channel syndrome causes severe weakness by novel mechanisms
4. New mutations in acetylcholine receptor subunit genes reveal heterogeneity in the slow-channel congenital myasthenic syndrome
5. A ?-subunit mutation in the acetylcholine receptor channel gate causes severe slow-channel syndrome
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1. Mitochondrial Mutations Can Alter Neuromuscular Transmission in Congenital Myasthenic Syndrome and Mitochondrial Disease;International Journal of Molecular Sciences;2023-05-09
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3. “Calcium bombs” as harbingers of synaptic pathology and their mitigation by magnesium at murine neuromuscular junctions;Frontiers in Molecular Neuroscience;2022-07-26
4. A bioassay for neuromuscular junction-restricted complement activation by myasthenia gravis acetylcholine receptor antibodies;Journal of Neuroscience Methods;2022-05
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