Clathrin-mediated endocytosis Sample Clauses

Clathrin-mediated endocytosis. The major and best characterized pathway is clathrin-mediated endocytosis (Xxxxx, X. and X. Xxxxxx, 2001, Xxxxxx, C. and X.X. Xxxxxx, 1995), which commonly mediates the uptake of plasma membrane receptors such as receptors of transferrin, epidermal growth factor (EGFR) and low density lipoproteins (LDLR) (Xxxxxx, X.X., 2008). This uptake process is receptor-mediated as it involves specific receptors located in invaginations of the plasma membrane known as clathrin-coated pits. These vesicles are characterized by the presence of a polyglonal clathrin coat and range in size from approximately 100 to 150 nm (Xxxxx, K. and X. Xxxxxx, 2001). They carry ligand-bound receptors inside the cell involving GTPase dynamin activity (Benmerah, A. and X. Xxxxxx, 2007) and they are transformed into early endosomes where the ligand is separated from the receptor. The ligand is then transferred to late endosomes for potential degradation in lysosomes. The receptors are recycled and transported back to the cellular membrane (Xxxxxx, I.A. et al., 2006). Genes internalized through the clathrin pathway end up in lysosomes for potential degradation, thus for a successful delivery of biologically active genes, lysosomal escape and release in the cytoplasm is crucial. This receptor-mediated endocytosis is energy-dependent and can be strongly inhibited by lowering temperature (Xxxxxxx T, X.X., 1991, Xxxxxx X. Xxxx, A.L.H., And Xxxxxx X. Xxxxxxx, 1980) or by depletion of the ATP pool using metabolic inhibitors (Xxxxxx, I.A. et al., 2006). In addition reagents that prevent the assembly of the clathrin lattice on the membrane specifically inhibit this pathway. Such treatments include potassium depletion (Xxxxxx, X.X. xx al., 1983, Xxxxxx, X.X., 2008), hypertonicity, cytosol acidification and the cationic amphipathic drug chloropromazine (Xxxx, X.X. xx al., 1993, Xxxxxx, I.A. et al., 2006, Xxxxxx, X.X., 2008).
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