CORDIS Project
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This project aims to investigate the mechanisms of clathrin-independent endocytosis driven by the protein endophilin-A3, focusing on its role in cancer progression and viral entry. It seeks to identify cellular regulators and small molecule inhibitors to manipulate this pathway.
In addition to classical clathrin-mediated endocytosis, mammalian cells have clathrin-independent endocytic (CIE) mechanisms.
Among others, the BAR domain proteins, that sense and induce membrane curvature, are key players in CIE.
In particular, the BAR domain protein endophilin-A3 (endoA3) drives CIE of the cell adhesion molecules CD166, L1CAM, and DICAM, with implications in tumour progression and viral infection.
The regulation, mechanism, and functional implications of this recently-identifi…
UNIVERSITE DE NAMUR
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