@misc{10481/110957,
year = {2017},
month = {12},
url = {https://hdl.handle.net/10481/110957},
abstract = {Synaptic transmission is critically dependent on synaptic vesicle (SV) recycling. Although the precise mechanisms of SV retrieval are still debated, it is widely accepted that a fundamental role is played by clathrin-mediated endocytosis, a form of endocytosis that capitalizes on the clathrin/adaptor protein complex 2 (AP2) coat and several accessory factors. Here, we show that the previously uncharacterized protein KIAA1107, predicted by bioinformatics analysis to be involved in the SV cycle, is an AP2-interacting clathrin-endocytosis protein (APache). We found that APache is highly enriched in the CNS and is associated with clathrin-coated vesicles via interaction with AP2. APache-silenced neurons exhibit a severe impairment of maturation at early developmental stages, reduced SV density, enlarged endosome-like structures, and defects in synaptic transmission, consistent with an impaired clathrin/AP2-mediated SV recycling. Our data implicate APache as an actor in the complex regulation of SV trafficking, neuronal development, and synaptic plasticity.},
publisher = {Cell Press},
keywords = {AP2, synaptic vesicles, endocytosis, apache},
title = {APache is an AP2-interacting protein involved in synaptic vesicle trafficking and neuronal development},
doi = {10.1016/j.celrep.2017.11.073 External Link},
author = {Piccini, Alessandra and Castroflorio, Enrico and Valente, Pierluigi and Guarnieri, Fabrizia C and Aprile, Davide and Michetti, Caterina and Bramini, Mattia and Giansante, Giorgia and Pinto, Bruno and Savardi, Annalisa and Cesca, Fabrizia and Bachi, Angela and Cattaneo, Angela and Wren, Jonathan D and Fassio, Anna and Valtorta, Flavia and Benfenati, Fabio and Giovedì, SIlvia},
}