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Third, antigenic modulation accelerates AChR internalization and lysosomal degradation through antibody-induced receptor cross-linking, reducing functional receptor density at the neuromuscular junction by approximately 70%90% ( Figure 1 2.1.2 Anti-muscle-specific kinase antibodies Myasthenia gravis mediated by anti-muscle-specific kinase antibodies (MuSK-Ab) exhibits distinct pathogenic mechanisms compared to AChR-MG

Kinesin, a motor protein responsible for anterograde transport of organelles, vesicles, and protein complexes from the cell body to synaptic terminals, causes transport disruption when mutated

This surface adsorption effect is more pronounced with lower peptide concentrations