Clathrin-mediated endocytosis pathway (CME pathway)

Clathrin-mediated endocytosis (CME) is a fundamental cellular pathway responsible for the internalization of extracellular molecules, membrane proteins, and lipids through the formation of clathrin-coated vesicles at the plasma membrane[4][7][9]. It is involved in diverse processes such as signal transduction (for G-protein and tyrosine kinase receptors), nutrient uptake (e.g., transferrin, LDL), synaptic vesicle recycling, and antigen presentation[2][4][8]. The process is orchestrated by the assembly of clathrin triskelions, adaptor proteins (such as AP-2), and dynamin, which together drive membrane curvature, vesicle budding, and scission[4][2][3]. While CME is a validated route for delivering drugs, pathogens, and nanoparticles into cells, the pathway itself is not a discrete molecular target, but rather a complex, conserved cellular process regulated by numerous proteins and lipids[8][1]. Disruption of CME has been implicated in various diseases, including cancer, neurodegenerative disorders, and infection[2][6].

Other names

Clathrin-mediated endocytosisCMEClathrin-dependent endocytosis

Inhibition of clathrin assembly or coat disassembly; Blocking dynamin-mediated vesicle scission; Modulation of adaptor protein complex function.