How does the binding of a ligand to a receptor cause it to become concentrated into a coated pit? Not all receptors that carry out receptor mediated endocytosis are found in coated pits prior to ligand binding yet they do end up in coated pits prior to becoming internalized

Binding of a ligand to its receptor produces a conformational change in the receptor initiating a sequence of reactions leading to a specific cellular response. Clustering/gathering of receptor proteins within coated pits is the first step of RME. This process may be either spontaneous or induced by ligands. Some receptors, such as those for LDL bearing cholesterol and transferrin bearing iron, appear to be clustered in coated pits independent of prior ligand binding. Other receptors, including those for EGF and insulin are evenly distributed over the plasma membrane.

The rate of receptor diffusion on the cell surface plasma membrane can explain their movement into coated pits.

Some studies have also suggested that membrane lipids flow toward coated pit areas and that this way all membrane proteins may be carried passively to coated pits, preferentially selecting for receptor proteins mediating endocytosis. These proteins may then become "trapped" via specific signals in the cytoplasmic tail (downstream effectors) which interact with structural components of the coated pit which includes the adaptor proteins- AP-2.