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.
Original language | English |
---|---|
Pages (from-to) | 120-129 |
Number of pages | 10 |
Journal | Current Opinion in Cell Biology |
Volume | 71 |
Early online date | 13 Apr 2021 |
DOIs | |
Publication status | Published - Aug 2021 |
Keywords
- Activity-dependent bulk endocytosis
- Cargoes
- Clathrin
- Clathrin-independent carriers/GPI-AP-enriched early endosomal compartments (CLIC/GEEC)
- Clathrin-independent endocytosis
- Clathrin-mediated endocytosis
- EGFR Non-Clathrin endocytosis
- Endocytosis
- Endophilin-A3/Galectin-8-mediated endocytosis
- Fast endophilin-mediated endocytosis (FEME)
- Glycolipid-Lectin hypothesis
- Glycosylphosphatidylinositol-anchored proteins
- Interleukin-2 receptor endocytosis
- Lipids
- Macropinocytosis
- Massive Endocytosis
- Receptors
- Ultrafast endocytosis