| Institution: | 1. Biochemistry and Cellular Biology Research Unit (URBC), Namur Research Institute for Life Science (NARILIS), University of Namur, Rue de Bruxelles 61, B-50000, Namur, Belgium;2. Institute of Structural and Molecular Biology, University College London, Gower Street, London, WC1E 6BT, UK;3. Institute of Structural and Molecular Biology, Birkbeck College, Malet Street, London, WC1E 7HX, UK;1. Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Robert-Rössle-Straße 10, 13125 Berlin, Germany;2. Freie Universität Berlin, Faculty of Biology, Chemistry, Pharmacy, 14195 Berlin, Germany;1. Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Robert-Roessle-Straße 10, 13125, Berlin, Germany;2. Department of Nanophysiology, Technische Universität Kaiserslautern, Paul-Ehrlich-Straße 23, 67663, Kaiserslautern, Germany;1. Carl-Ludwig-Institute for Physiology, Medical Faculty, University of Leipzig, Liebigstrasse 27, 04103 Leipzig, Germany;2. The Vollum Institute, Oregon Health & Science University, Portland, OR 97239, USA;1. Department of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, 06520-8002, USA;2. Howard Hughes Medical Institute and Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA, 02115, USA;1. Cardiac and Cerebral Vascular Research Center, Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China;2. Faculty of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China;3. Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China |
| Abstract: | Endocytosis mediates the uptake of extracellular proteins, micronutrients and transmembrane cell surface proteins. Importantly, many viruses, toxins and bacteria hijack endocytosis to infect cells. The canonical pathway is clathrin-mediated endocytosis (CME) and is active in all eukaryotic cells to support critical house-keeping functions. Unconventional mechanisms of endocytosis exit in parallel of CME, to internalize specific cargoes and support various cellular functions. These clathrin-independent endocytic (CIE) routes use three distinct mechanisms: acute signaling-induced membrane remodeling drives macropinocytosis, activity-dependent bulk endocytosis (ADBE), massive endocytosis (MEND) and EGFR non-clathrin endocytosis (EGFR-NCE). Cargo capture and local membrane deformation by cytosolic proteins is used by fast endophilin-mediated endocytosis (FEME), IL-2Rβ endocytosis and ultrafast endocytosis at synapses. Finally, the formation of endocytic pits by clustering of extracellular lipids or cargoes according to the Glycolipid-Lectin (GL-Lect) hypothesis mediates the uptake of SV40 virus, Shiga and cholera toxins, and galectin-clustered receptors by the CLIC/GEEC and the endophilin-A3-mediated CIE. |
