Additionally, functional blockade of nAChRs with MG sera and/or subunit-specific mAb in myotubes led to transcriptional upregulation of α-actin and desmin (muscle specific proteins related to contractile machinery), complement components C1s, C3aR, C5, and C9, and also an observed trend of enhanced expression of nAChR and VGCC subunits.
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Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.
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