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Updated: Feb 16, 2026

A High-content Assay for Monitoring AMPA Receptor Trafficking
Published on: January 28, 2019
APache Is an AP2-Interacting Protein Involved in Synaptic Vesicle Trafficking and Neuronal Development
Alessandra Piccini1, Enrico Castroflorio2, Pierluigi Valente1
1Department of Experimental Medicine, University of Genova, 16132 Genova, Italy.
A newly discovered protein, APache, is crucial for synaptic vesicle recycling in the central nervous system (CNS). Its absence impairs neuronal development and synaptic transmission by disrupting clathrin-mediated endocytosis.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Synaptic vesicle (SV) recycling is essential for synaptic transmission.
- Clathrin-mediated endocytosis, involving clathrin/adaptor protein complex 2 (AP2), is a key SV retrieval mechanism.
- The precise molecular players in SV recycling are still under investigation.
Purpose of the Study:
- To characterize the function of the uncharacterized protein KIAA1107 in synaptic vesicle recycling.
- To determine the role of KIAA1107 in neuronal development and synaptic transmission.
Main Methods:
- Bioinformatic analysis to predict protein function.
- Biochemical assays to identify AP2 interaction.
- Neuronal silencing experiments to assess APache function.
- Microscopy to evaluate SV density and endosomal structures.
Main Results:
- KIAA1107 identified as APache, an AP2-interacting clathrin-endocytosis protein.
- APache is enriched in the CNS and associates with clathrin-coated vesicles via AP2.
- APache-silenced neurons show impaired maturation, reduced SV density, and enlarged endosomes.
- Synaptic transmission is defective in APache-silenced neurons.
Conclusions:
- APache plays a critical role in clathrin/AP2-mediated SV recycling.
- APache is essential for proper neuronal development and synaptic function.
- The findings implicate APache in the regulation of SV trafficking, neuronal plasticity, and development.
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