Due to this evidence of an alternative mechanism for MoDE 3 uptake, we tested several classes of endocytosis inhibitors including clathrin-dependent (monensin), endosomal acidification (bafilomycin, ammonium chloride), caveolae-mediated (genistein, nystatin), micropinocytosis (EIPA, amiloride) and phagocytosis (cytochalasin D) (Figure ) to determine which processes contributed to uptake. A significant decrease in cellular uptake of the streptavidin target protein was observed for cytochalasin D, monensin and bafilomycin. This pattern of inhibition profile is consistent with critical involvement of clathrin, actin polymerization, endosomal acidification and receptor recycling in the endocytic mechanism and is not consistent with alternative processes such as macropinocytosis and caveolae-mediated endocytosis.