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The overall goal of this proposal is to elucidate the molecular pathway that mediates SV protein degradation in mammalian glutamatergic neurons.
Our previous studies have identified three potential components of this pathway (the E3 ubiquitin ligase Siah1, the endosomal sorting complex required for transport (ESCRT) system, and the small GTPase Rab35), and this project will evaluate their roles in facilitating SV protein degradation.
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We will further assess whether pathological activation of this pathway disrupts SV-stasis and triggers synapse degeneration.