receptor-mediated endocytosis

Some materials are incorporated into the endosome by receptor-mediated endocytosis. Some extracellular molecules bind to transmembrane receptor proteins that efficiently accumulate in coated pits. One example of receptor-mediated endocytosis important in human physiology is the main mechanism by which cholesterol is taken up by cells, in particular, liver cells.

In some people, the cholesterol receptor is defective, so uptake of cholesterol from the blood into liver cells is slow and cholesterol accumulates in the blood. This is thought to be the cause of damage to blood vessel walls, as increased cholesterol levels have also been observed in cases of atherosclerosis. Because further research into this process may prove that arterial damage causes cholesterol receptor damage, rather than vice versa, a plausible explanation for the occurrence of strokes and heart attacks at a young age would present itself.

One great risk with very high LDL levels is that LDL is vulnerable to free-radical damage and that damaged LDL molecules could clump together and form arterial blockages, especially if encountering the sticky platelets of already-damaged blood vessel walls.

Short-signal peptides that target certain transmembrane proteins into clathrin-coated pits have been identified. A set of proteins called adaptins bind the signal peptides. The signal for the cholesterol receptor is the tetrapeptide Asn-Pro-Val-Tyr.

Another example of receptor-mediated endocytosis involves the actions of the cell surface transferrin receptor, which binds the iron transport protein transferrin. In the acidic endosome, the iron is released from transferrin, and then the iron-free transferrin (still bound to the transferrin receptor) returns from the early endosome to the cell surface.

See also

 endocytosis