Myasthenia gravis (MG) is a neuromuscular junction disorder that involves several dysfunctions that eventually lead to muscle fatigue and weakness. Although immunotherapeutics are considered an effective treatment option for MG, treatment-refractory cases are documented. In this case report, we evaluate the efficacy and safety of rituximab in treating three cases of myasthenia gravis admitted to the neurology department of a tertiary hospital.
View Article and Find Full Text PDFHere, we show that the cellular DNA replication protein and ATR substrate SMARCAL1 is recruited to viral replication centers early during adenovirus infection and is then targeted in an E1B-55K/E4orf6- and cullin RING ligase-dependent manner for proteasomal degradation. In this regard, we have determined that SMARCAL1 is phosphorylated at S123, S129, and S173 early during infection in an ATR- and CDK-dependent manner, and that pharmacological inhibition of ATR and CDK activities attenuates SMARCAL1 degradation. SMARCAL1 recruitment to viral replication centers was shown to be largely dependent upon SMARCAL1 association with the RPA complex, while Ad-induced SMARCAL1 phosphorylation also contributed to SMARCAL1 recruitment to viral replication centers, albeit to a limited extent.
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